WO2022115581A1

WO2022115581A1 - Methods for treating infertility and/or endometriosis comprising ex-527

Info

Publication number: WO2022115581A1
Application number: PCT/US2021/060787
Authority: WO
Inventors: Steven Young; Bruce Lessey; Jae-Wook Jeong
Original assignee: The University Of North Carolina At Chapel Hill; Prisma Health; Board Of Trustees Of Michigan State University
Priority date: 2020-11-25
Filing date: 2021-11-24
Publication date: 2022-06-02

Abstract

The presently disclosed subject matter pertains in some embodiments to methods and compositions for use in the detection, management and/or treatment of endometriosis and/or subfertility/infertility using SIRT1 inhibitor EX-527.

Description

METHODS FOR TREATING INFERTILITY AND/OR ENDOMETRIOSIS COMPRISING EX-527 STATEMENT OF PRIORITY This application claims the benefit, under 35 U.S.C. § 119(e), of U.S. Provisional Application No. 63/118302, filed on November 25, 2020, the entire contents of which are incorporated by reference herein. STATEMENT OF GOVERNMENT SUPPORT This invention was made with government support under Grant Number R01 HD084478 awarded by the National Institutes of Health. The government has certain rights in the invention. FIELD OF THE INVENTION The presently disclosed subject matter pertains in some embodiments to methods and compositions for use in the detection, management and/or treatment of endometriosis and/or subfertility/infertility using SIRT1 inhibitor EX-527. BACKGROUND OF THE INVENTION In Vitro Fertilization (IVF) is a commonly used procedure with about 284,385 cycles completed in 2017. Non-donor egg success rates for all ages resulting in live births for 2016 were only 21.3% overall. Including the best prognosis group, younger than 35, pregnancy rates and live birth rates were still only 52.9% and 45.7%, respectively. The cases that fail to implant or miscarry after implantation, especially with normal euploid embryos, are often unexplained. Endometriosis or "unknown factors" account for 67.4% of cases overall; in 2016 where complete data are available 86,237 cycle starts using non-donor oocytes, only 19,137 resulted in live birth. Now with availability of reliable biomarkers for the presence of endometriosis, we recognize that 70% of unexplained IVF failures test positive for SIRT1 and BCL6, and appropriate treatments can reverse infertility and pregnancy losses. Unfortunately, recognized treatments for implantation failure in IVF are limited, and have many side effects. They include menopause-inducing gonadotropin-releasing hormone agonist therapy (GnRHa) combined with aromatase inhibitors (letrozole), that are associated with bone loss and hot flashes. Endometrial receptivity defects are increasingly not recognized or treated due to a reduction in the utilization of laparoscopic surgery, explaining why pregnancy rates have plateaued in the setting of Assisted Reproductive Technologies (ART). Based on the conservative estimate of 50,000 IVF failures per year due to endometriosis or other inflammatory conditions; at a conservative estimate of $10,000 per attempt, the cost to society in the USA alone is over $500 million dollars. The emotional cost and loss productivity may be far greater. SUMMARY OF THE INVENTION One aspect of the present invention comprises a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a BCL6 gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject and also has a level of expression of the BCL6 gene product that is greater than the level of expression of the BCL6 gene product of the control subject; and g) administering to the subject an effective amount of EX- 527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) detecting a level of expression of a BCL6 gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product detected in (d); f) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject obtained and an HSCORE calculated for a level of expression of a BCL6 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method for increasing the likelihood of implantation of an embryo in a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene product and a BCL6 gene product, comprising administering to the subject having overexpression of a SIRT1 gene product and a BCL6 gene product an effective amount of EX-527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method of treating infertility in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product and a BCL6 gene product an effective amount of EX-527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method of treating endometriosis in a subject in need thereof, comprising administering to a subject, optionally a subject having overexpression of a SIRT1 gene product and a BCL6 gene product, an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a BCL6 gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and has a level of expression of the BCL6 gene product that is greater than the level of expression of the BCL6 gene product of the control subject; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) detecting a level of expression of a BCL6 gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression detected in (d); f) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject an HSCORE calculated for the level of expression of a BCL6 gene product that is greater than a pre-determined cut-off value; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a BCL6 gene product in a sample of endometrium obtained from a control subject during the second half of said control subject’s menstrual cycle; f) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and a level of expression of the BCL6 gene product greater than the level of expression of the BCL6 gene product of the control subject; g) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a BCL6 gene product in the subsequent sample; and k) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (i) and comparing the level of expression of the BCL6 gene product detected in (c) with the level of expression of the BCL6 gene product detected in (j), wherein a decrease in (i) relative to (b) and a decrease in (j) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (i) relative to (b) and an increase or no change in (j) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a BCL6 gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the first sample; f) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value and an HSCORE based on the level of expression of the BCL6 gene product that is greater than a pre-determined cut-off level; g) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; k) detecting a level of expression of a BCL6 gene product in the subsequent sample; l) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the subsequent sample; and m) comparing the HSCORE of (c) with the HSCORE of (j) and comparing the HSCORE of (e) with the HSCORE of (l), wherein a decrease in the HSCORE of (j), along with a decrease in the HSCORE of (l) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (j) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (l) indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the present invention provides a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject and also has a level of expression of the K-ras gene product that is greater than the level of expression of the K-ras gene product of the control subject; and g) administering to the subject an effective amount of EX- 527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) detecting a level of expression of a K-ras gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product detected in (d); f) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject obtained and an HSCORE calculated for a level of expression of a K-ras gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method for increasing the likelihood of implantation of an embryo in a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene product and a K-ras gene product, comprising administering to the subject having overexpression of a SIRT1 gene product and a K-ras gene product an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of treating infertility in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product and a K-ras gene product an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of treating endometriosis in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product and a K-ras gene product an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and has a level of expression of the K-ras gene product that is greater than the level of expression of the K- ras gene product of the control subject; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) detecting a level of expression of a K-ras gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression detected in (d); f) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject an HSCORE calculated for the level of expression of a K-ras gene product that is greater than a pre-determined cut-off value; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject during the second half of said control subject’s menstrual cycle; f) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and a level of expression of the K-ras gene product greater than the level of expression of the K-ras gene product of the control subject; g) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a K-ras gene product in the subsequent sample; and k) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (i) and comparing the level of expression of the K-ras gene product detected in (c) with the level of expression of the K-ras gene product detected in (j), wherein a decrease in (i) relative to (b) and a decrease in (j) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (i) relative to (b) and an increase or no change in (j) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a K-ras gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the first sample; f) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value and an HSCORE based on the level of expression of the K-ras gene product that is greater than a pre-determined cut-off level; g) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; k) detecting a level of expression of a K-ras gene product in the subsequent sample; l) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the subsequent sample; and m) comparing the HSCORE of (c) with the HSCORE of (j) and comparing the HSCORE of (e) with the HSCORE of (l), wherein a decrease in the HSCORE of (j), along with a decrease in the HSCORE of (l) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (j) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (l) indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin- releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) detecting a level of expression of a K-ras gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f) and comparing the level of expression of the K-ras gene product detected in (c) with the level of expression of the K-ras gene product detected in (g), wherein a decrease in (f) relative to (b) and a decrease in (g) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) and an increase or no change in (g) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a K-ras gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the first sample; f) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; g) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (f); h) detecting a level of expression of a SIRT1 gene product in the subsequent sample; i) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a K-ras gene product in the subsequent sample; k) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the subsequent sample; and l) comparing the HSCORE of (c) with the HSCORE of (i) and comparing the HSCORE of (e) with the HSCORE of (k), wherein a decrease in the HSCORE of (i), along with a decrease in the HSCORE of (k) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (i) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (k) indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with an effective amount of a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) detecting a level of expression of a BCL6 gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f) and comparing the level of expression of the BCL6 gene product detected in (c) with the level of expression of the BCL6 gene product detected in (g), wherein a decrease in (f) relative to (b) and a decrease in (g) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) and an increase or no change in (g) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a BCL6 gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the first sample; f) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; g) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (f); h) detecting a level of expression of a SIRT1 gene product in the subsequent sample; i) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a BCL6 gene product in the subsequent sample; k) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the subsequent sample; and l) comparing the HSCORE of (c) with the HSCORE of (i) and comparing the HSCORE of (e) with the HSCORE of (k), wherein a decrease in the HSCORE of (i), along with a decrease in the HSCORE of (k) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (i) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (k) indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the present invention provides a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject and also has a level of expression of the K-ras gene product that is greater than the level of expression of the K-ras gene product of the control subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) detecting a level of expression of a K-ras gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product detected in (d); f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject obtained and an HSCORE calculated for a level of expression of a K-ras gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K- ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of treating endometriosis derived ovarian cancer in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product and a K-ras gene product an effective amount of EX-527, optionally in combination with a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject during the second half of said control subject’s menstrual cycle; f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and a level of expression of the K-ras gene product greater than the level of expression of the K-ras gene product of the control subject; g) treating the endometriosis derived ovarian cancer by administering to the subject an effective amount of EX-527, optionally in combination with a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a K-ras gene product in the subsequent sample; and k) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (i) and comparing the level of expression of the K-ras gene product detected in (c) with the level of expression of the K-ras gene product detected in (j), wherein a decrease in (i) relative to (b) and a decrease in (j) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (i) relative to (b) and an increase or no change in (j) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a K-ras gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the first sample; f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value and an HSCORE based on the level of expression of the K-ras gene product that is greater than a pre-determined cut-off level; g) treating the endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with a K- ras inhibitor, a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; k) detecting a level of expression of a K-ras gene product in the subsequent sample; l) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the subsequent sample; and m) comparing the HSCORE of (c) with the HSCORE of (j) and comparing the HSCORE of (e) with the HSCORE of (l), wherein a decrease in the HSCORE of (j), along with a decrease in the HSCORE of (l) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (j) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (l) indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre- determined cut-off value, as measured in a sample of endometrium from the subject obtained; and e) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method for increasing the likelihood of implantation of an embryo in a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene, comprising administering to the subject having overexpression of a SIRT1 gene an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of treating infertility in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of treating endometriosis in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and e) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and e) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; d) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and g) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f), wherein a decrease in (f) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value; e) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX- 527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; h) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and i) comparing the HSCORE of (c) with the HSCORE of (h), wherein a decrease in the HSCORE of (h) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (h) to a value greater than or equal to a pre- determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises a method of managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; d) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (c); e) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and f) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (e), wherein a decrease in (e) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (e) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and h) comparing the HSCORE of (c) with the HSCORE of (g), wherein a decrease in the HSCORE of (g) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (g) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; d) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (c); e) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and f) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (e), wherein a decrease in (e) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (e) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and h) comparing the HSCORE of (c) with the HSCORE of (g), wherein a decrease in the HSCORE of (g) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (g) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and e) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and e) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of treating endometriosis derived ovarian cancer in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject, optionally obtained during the first and/or second half (e.g., secretory phase and/or proliferative phase) of the subject's menstrual cycle; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject, optionally obtained during the first and/or the second half (e.g., secretory phase and/or proliferative phase) of the subject's menstrual cycle; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; e) treating the endometriosis derived ovarian cancer by administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (g), wherein a decrease in (g) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (g) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value; e) treating the endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; h) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and i) comparing the HSCORE of (c) with the HSCORE of (h), wherein a decrease in the HSCORE of (h) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (h) to a value greater than or equal to a pre- determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. BRIEF DESCRIPTION OF THE DRAWINGS FIG.1 shows histology (panel A) and a bar graph (panel B) of inhibition of endometriosis development by EX-527 in the mouse model described herein. FIG.2 shows representative images of GD5.5 Pgr^cre/+ Sirt1-LSL mice that conditionally over-express SIRT in the uterus. These mice are infertile and display a profound implantation defect (upper images). When those mice are treated with EX-527 (50 ug/mouse) implantation is restored (lower images). FIGS.3A-3B show the expression of SIRT1 in mouse uterus during early pregnancy and the menstrual model. FIG.3A shows a schematic diagram for the mouse menstrual model. The expression of SIRT1 at gestation day (GD) 2.5 (panel a), GD 3.5 (panel b), menstrual-like tissues of mouse (panel c), and without primary antibody (panel d). The quantification data of immunohistochemistry SIRT1 in mouse. The data represents the mean ± standard error of the mean. ***P < 0.001. Abbreviations: Endo Sec, endometrium from secretory phase; Endo Prolif, endometrium from proliferative phase. FIG.3B shows immunohistological images from additional time gestation day (GD) timepoints. FIG.4 shows the effect of SIRT1 over-expression on endometriosis development. FIGS.5A-5B images of histology and quantified data related thereto of the Sirt1^over mouse model. FIG.5A shows the phenotype of implantation failure in Sirt1 over-expression is rescued by EX-527. FIG.5B shows uterus-specific overexpression of Sirt1 causes implantation failure and decidualization defect. The overexpression of SIRT1 was evaluated in the uteri of control and Sirt1Over at gestation day (GD) 3.5 by quantitative real-time polymerase chain reaction (FIG.5B panel A) and immunohistochemical analysis and quantification data of SIRT1 positive cell (FIG.5B panel B). (FIG.5B panel C) The implantation failure was observed in Sirt1^Over mice at GD 7.5. (FIG.5B panel D) The schematic diagrams for artificial decidualization and gross anatomy of artificially induced decidualized uteri of control (a) and Sirt1Over (b) mice. There was a significant decrease in stimulated and unstimulated (control) horn weight ratio in Sirt1^Over mice as compared with control. The data represent the mean ± standard error of the mean. **P < 0.01. FIGS.6A-6B shows SIRT1 through the cycle in normal controls and women with endometriosis. FIG.6A shows a data graph of the quantification data of immunohistochemistry SIRT1 in human as an H-Score. FIG.6B shows histology images from human samples as labeled panels a)-h). The expression of SIRT1 proteins was examined by immunohistochemistry at proliferative (panels a and e), secretory (panels b and f), menses (panels c and g), and without primary antibody (panels d and h) tissues from women without endometriosis (panels a-d) and in women with endometriosis (panels e-h). The quantification data of immunohistochemistry SIRT1 in human. FIG.7 shows images and quantified data plots indicating Uterus-specific overexpression of Sirt1 results in nonreceptive endometrium due to progesterone resistance. (FIG.7 panel A) Immunohistochemical analysis of Ki67 proteins and (FIG.7 panel B) quantification data of Ki67-positive cells at gestation day (GD) 3.5 in endometrium of control (image a) and Sirt1Over (image b) mice. quantitative real-time polymerase chain reaction analysis of (FIG.7 panel C) estrogen receptor 1 target genes (Muc-1, Clca3, Ltf) and (FIG.7 panel D) progesterone receptor target (PGR) genes (Fst, Klf15, Patch1, Gli1) in uteri of control and Sirt1Over mice. (FIG.7 panel E) The interaction between sirtuin-1 and progesterone receptor A. (FIG.7 panel F) Immunohistochemical analysis of PGR proteins and (FIG.7 panel G) HSCORE of PGR at GD 3.5 in endometrium of control (a) and Sirt1Over (b) mice. The results represent the mean ± standard error of the mean. ***P < 0.001; **P < 0.01; *P < 0.05. FIG.8 shows images and quantified data indicating that endometriosis induces sirtuin-1 (SIRT1) overexpression in the eutopic endometrium and Sirt1 overexpression in endometriotic lesion results in an increase of endometriosis development. (FIG.8 panel A) The expression of SIRT1 was significantly increased in mouse endometriosis (Eosis) group compared to sham group. (FIG.8 panel B) The quantification data of immunohistochemistry SIRT1 in mouse endometriosis model. (FIG.8 panel C) Autologous induction of endometriosis in control and Sirt1^Over mice showed (FIG.8 panel D) an increase of number of ectopic sites in Sirt1^Over mice compared to control. The results represent the mean ± standard error of the mean. ***P < 0.001; *P < 0.05. FIG.9 shows images and quantified data indicating that EX-527 restores implantation failure in Sirt1^Over mice and suppresses endometriosis development in mouse. (FIG.9 panel A) EX-527 at dose of 0.5 mg/ kg treatment did not harm female reproduction functions. (FIG.9 panel B) EX-527 treatment at dose of 2.5 mg/kg rescued an implantation failure observed in Sirt1^Over mice. (FIG.9 panel C) EX-527 treatment at dose of 0.5 mg/kg reduced the development of endometriotic sites in mouse endometriosis model. The results represent the mean ± standard error of the mean. **P < 0.01. DETAILED DESCRIPTION The present invention now will be described hereinafter with reference to the accompanying drawings and examples, in which embodiments of the invention are shown. This description is not intended to be a detailed catalog of all the different ways in which the invention may be implemented, or all the features that may be added to the instant invention. For example, features illustrated with respect to one embodiment may be incorporated into other embodiments, and features illustrated with respect to a particular embodiment may be deleted from that embodiment. Thus, the invention contemplates that in some embodiments of the invention, any feature or combination of features set forth herein can be excluded or omitted. In addition, numerous variations and additions to the various embodiments suggested herein will be apparent to those skilled in the art in light of the instant disclosure, which do not depart from the instant invention. Hence, the following descriptions are intended to illustrate some particular embodiments of the invention, and not to exhaustively specify all permutations, combinations, and variations thereof. Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. The terminology used in the description of the invention herein is for the purpose of describing particular embodiments only and is not intended to be limiting of the invention. All publications, patent applications, patents and other references cited herein are incorporated by reference in their entireties for the teachings relevant to the sentence and/or paragraph in which the reference is presented. Unless the context indicates otherwise, it is specifically intended that the various features of the invention described herein can be used in any combination. Moreover, the present invention also contemplates that in some embodiments of the invention, any feature or combination of features set forth herein can be excluded or omitted. To illustrate, if the specification states that a composition comprises components A, B and C, it is specifically intended that any of A, B or C, or a combination thereof, can be omitted and disclaimed singularly or in any combination. As used in the description of the invention and the appended claims, the singular forms "a," "an" and "the" are intended to include the plural forms as well, unless the context clearly indicates otherwise. Also as used herein, "and/or" refers to and encompasses any and all possible combinations of one or more of the associated listed items, as well as the lack of combinations when interpreted in the alternative ("or"). The term "about," as used herein when referring to a measurable value such as an amount or concentration and the like, is meant to encompass variations of ± 10%, ± 5%, ± 1%, ± 0.5%, or even ± 0.1% of the specified value as well as the specified value. For example, "about X" where X is the measurable value, is meant to include X as well as variations of ± 10%, ± 5%, ± 1%, ± 0.5%, or even ± 0.1% of X. A range provided herein for a measurable value may include any other range and/or individual value therein. As used herein, phrases such as "between X and Y" and "between about X and Y" should be interpreted to include X and Y. As used herein, phrases such as "between about X and Y" mean "between about X and about Y" and phrases such as "from about X to Y" mean "from about X to about Y." The term "comprise," "comprises" and "comprising" as used herein, specify the presence of the stated features, integers, steps, operations, elements, and/or components, but do not preclude the presence or addition of one or more other features, integers, steps, operations, elements, components, and/or groups thereof. As used herein, the transitional phrase "consisting essentially of" means that the scope of a claim is to be interpreted to encompass the specified materials or steps recited in the claim and those that do not materially affect the basic and novel characteristic(s) of the claimed invention. Thus, the term "consisting essentially of" when used in a claim of this invention is not intended to be interpreted to be equivalent to "comprising." As used herein, the term "BCL6" refers to the B-cell lymphoma 6 gene (also referred to as the B-cell CLL/lymphoma 6 gene; gene symbol BCL6) as well as gene products encoded and/or derived therefrom. In humans, the BCL6 gene is present on chromosome 3. The term "BCL6" also corresponds to orthologs of human BCL6 from other species. As used herein, the terms "sirtuin 1" and "SIRT1" refers to the sirtuin 1gene (gene symbol SIRT1) as well as gene products encoded and/or derived therefrom. In humans, the SIRT1 gene is present on chromosome 10. Exemplary human SIRT1 gene products include, but are not limited to the nucleotide sequences disclosed in the GENBANK® Accession Nos. NM_012238 and NM_001142498 , which encode the amino acid sequences disclosed in GENBANK® Accession Nos. NP_036370 and NP_001135970 , respectively. The term "SIRT1" also corresponds to orthologs of human SIRT1 from other species, including but not limited to Gorilla, mouse, rat, Sus scrofa, Bos taurus, Felis cattus Canis lupus familiaris, Pan troglodytes, Equus caballus, Macaca mulatta, Pongo abelii, and any other GENBANK® SIRT1 orthologs. As used herein, the term "subject" refers to any animal, including but not limited to any mammal, such as but not limited to humans, non-human primates, rodents, and the like, which is to be the recipient of a particular treatment. The terms "subject" and "patient" are in some embodiments used interchangeably herein, such as but not limited to in reference to a human subject or patient. As used herein, the term "sample" is used in its broadest sense. In one sense, it is meant to include a specimen from a biological source. Biological samples can be obtained from animals (including humans) and encompass fluids (e.g., blood, mucus, urine, saliva), solids, tissues, cells, and gases. The sample can comprise fluids or washings of the uterine lining or sample prepared by similar techniques involving cervical lavage or brushings. The sample may be collected during any stage of the subject's cycle, e.g., the secretory and/or the proliferative stage. A sample of this invention can be any biological sample in which BCL6, SIRT1, and/or KRAS genes and/or proteins can be detected. Nonlimiting examples of a sample of this invention include blood, serum, plasma, endometrium, cervical swab, saliva, tears, vaginal secretion, urine, any body fluid, breast milk or secretion, exudate, secretion, lavage, washing, tissue, biological matter, cavity fluid and the like. As used herein, the term "fertility treatment’ refers to any procedure, therapy or protocol to facilitate and/or increase the likelihood of fertilization. Nonlimiting examples of a fertility treatment of this invention include in vitro fertilization (IVF), frozen embryo transplant (FET), fresh embryo transplant, intrauterine insemination, artificial insemination, fertility drugs, assisted reproductive technology (ART), intracytoplasmic sperm injection (ICSI), gamete intrafallopian tube transfer (GIFT), zygote intrafallopian tube transfer (ZIFT), donor egg transfer, timed intercourse, etc., as are known in the art. As used herein, the term "endometriosis derived ovarian cancer" refers to ovarian cancer derived from endometriosis or endometrial tissue. In some embodiments, the ovarian cancer can be a type 1 ovarian cancer. In some embodiments, the ovarian cancer can be endometrioid ovarian cancer. In some embodiments, the ovarian cancer can be clear cell ovarian cancer. Treatment of endometriosis derived ovarian cancer of this invention can comprise the treatments described herein and/or known treatments for ovarian cancer. Nonlimiting examples of treatment for endometriosis and/or endometriosis derived ovarian cancer include surgical removal of ectopic lesions and/or hormonal suppression focused on reducing estrogen, such as progestins, androgens, gonadotropin-releasing hormone (GnRH) agonists, and aromatase inhibitors, which are the current gold standards of therapy. ERK pathway inhibitors may also have a role in the treatment of endometriosis. Estrogen has been shown to increase SIRT1, paralleled by a decrease in PPAR-g. Indirectly, estrogen may be increased by activation of Cox2 and aromatase by IL17, thus aromatase inhibitors, estrogen antagonists or cytokine (IL17) inhibitors may each be potential therapeutic options for treatment. Aromatase inhibitors have been shown to improve IVF success rates in the setting of IVF specifically in women with endometrial receptivity problems. Thus anti-estrogens or even anti-androgens or other specific SERMs or SARMs might be useful to target this pathway, as well as other means to inhibit the AKT pathway. Other therapies may also target this pathway including doxycycline. As used herein, the phrase "recurrent pregnancy loss" (RPL) refers to a condition when a woman experiences two or more consecutive pregnancy losses prior to 20 weeks (see a discussion on the website of the American Society for Reproductive Medicine). RPL is a major health concern to women, affecting about 17% of couples wishing to have children. The diagnostic evaluation of RPL is extensive and complex, with many different etiologies, each causing a small proportion of the total cases. The etiologies can be grouped into five categories: anatomic, infectious, hormonal, immunological, and genetic, thereby requiring the collaborative efforts of many medical specialists. It has been estimated that the specific cause for RPL remains unknown in 37-79% of affected women (Stephenson, 1996). See also U.S. Patent No.6,268,145, incorporated herein by reference in its entirety. As used herein, the phrase "progesterone-resistance" (P-resistance) refers to a condition wherein normal levels of progesterone elicit a subnormal or reduced response. P- resistance can occur at the level of the progesterone receptor isoforms (PR-A and PR-B; Igarashi et al., 2005; Attia et al., 2000), steroid receptor co-activators, or downstream effectors (TGFβ, DKK-1, Retinoic acid, c-myc, etc.). In endometriotic lesions, a decrease in the expression of the progesterone target gene 17-beta hydroxysteroid dehydrogenase type I is evidence of P-resistance in ectopic endometrium (Vierikko et al., 1985; Bulun et al., 2006). Studies are conflicting regarding the normalcy of circulating levels of progesterone in women with endometriosis (Brosenset al., 1978; Cheesman et al., 1983; Williams et al., 1986; Kusuhara, 1992; Cunha-Filho et al., 2003), and this discrepancy may be secondary to difficulties in both ascertainment and interpretation of circulating progesterone levels. A single serum progesterone level may not be representative of luteal adequacy (Abraham et al., 1974; Laufer et al., 1982), and successful intrauterine pregnancy has been documented with mid-luteal P levels as low as 3-4 ng/ml (Costello et al., 2004). Finally, a study of luteal endometrial differentiation in programmed cycles of physiologic and subphysiologic exogenous progesterone replacement in GnRH agonist-suppressed healthy volunteers showed no differences in endometrial thickness, histology, or epithelial integrin expression at the lower serum progesterone level (Usadi et al., 2003). This finding supports the argument that the reduced progesterone response in the eutopic endometrium of women with endometriosis is an intrinsic biologic alteration of the endometrium. A model for progesterone resistance based on differential PR isoform expression has been described for ectopic endometrium (Bulun et al., 2006), and a reduced responsiveness to progesterone in eutopic endometrium has been implicated in disease pathogenesis (Osteen et al., 2005). See also U.S. Patent Nos. 7,871,778; 8,247,174; 9,175,349. As used herein, the terms "subfertility/infertility" "subfertility" and "infertility" and grammatical variations thereof, refer to the condition of being less than normally fertile, which can be further characterized as a prolonged period of non-conception. In some cases, a subfertile subject can still capable of effecting conception. However, in other cases, the term "subfertility" is also meant to encompass an infertile subject. The term "subfertility" can also pertain to a condition whereby a person can conceive but not successfully complete the pregnancy, as in miscarriage or recurrent abortion. The term "subfertility" is also meant to encompass difficulties with regard to embryo implantation, including but not limited to embryo implantation related to in vitro fertilization (IVF) treatment and/or with respect to frozen embryo transfer (FET). By the terms "treat," "treating" or "treatment of" (and grammatical variations thereof) it is meant that the severity of the subject’s condition is reduced, at least partially improved or stabilized and/or that some alleviation, mitigation, decrease or stabilization in at least one clinical symptom is achieved and/or there is a delay in the progression of the disease or disorder. The terms "prevent," "preventing" and "prevention" (and grammatical variations thereof) refer to prevention and/or delay of the onset of a disease, disorder and/or a clinical symptom(s) in a subject and/or a reduction in the severity of the onset of the disease, disorder and/or clinical symptom(s) relative to what would occur in the absence of the methods of the invention. The prevention can be complete, e.g., the total absence of the disease, disorder and/or clinical symptom(s). The prevention can also be partial, such that the occurrence of the disease, disorder and/or clinical symptom(s) in the subject and/or the severity of onset is less than what would occur in the absence of the present invention. A "treatment effective," "therapeutic," or "effective" amount as used herein is an amount that is sufficient to provide some improvement or benefit to the subject. Alternatively stated, a "treatment effective," "therapeutic," or "effective" amount is an amount that will provide some alleviation, mitigation, decrease or stabilization in at least one clinical symptom in the subject. Those skilled in the art will appreciate that the therapeutic effects need not be complete or curative, as long as some benefit is provided to the subject. A "prevention effective" amount as used herein is an amount that is sufficient to prevent and/or delay the onset of a disease, disorder and/or clinical symptoms in a subject and/or to reduce and/or delay the severity of the onset of a disease, disorder and/or clinical symptoms in a subject relative to what would occur in the absence of the methods of the invention. Those skilled in the art will appreciate that the level of prevention need not be complete, as long as some benefit is provided to the subject. As used herein, the terms "reduce," "reduces," "reduction" and similar terms mean a decrease of at least about 5%, 10%, 15%, 20%, 25%, 35%, 50%, 75%, 80%, 85%, 90%, 95%, 97%, 98%, 99%, 100% or more. As used herein, the terms "enhance," "enhances," "enhancement" and similar terms indicate an increase of at least about 10%, 20%, 25%, 50%, 75%, 100%, 150%, 200%, 300%, 400%, 500% or more. The term "administering" or "administration" of a composition and/or in a method of the present invention to a subject includes any route of introducing or delivering to a subject a compound to perform its intended function (e.g., for use in any one of the methods disclosed herein, e.g., for use in the treatment of infertility and/or endometriosis). Administration includes self-administration and the administration by another. In some embodiments, the results of the various antibody-based assays may be expressed in terms of a "histochemistry score", also known as an HSCORE. HSCOREs are expressions of antibody staining intensity, and are broadly discussed in Lessey et al., 1992. By way of example and not limitation, in some embodiments an HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100 where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. An HSCORE can function as a pre-determined cut-off such that expression above or below a pre-determined HSCORE in a particular subject for a particular biomarker can permit that subject’s status for that biomarker to be identified as "normal" vs. "abnormal", positive vs. negative, or any other discriminator. With respect to SIRT1, for example, in some embodiments an abnormal SIRT1 status may comprise an HSCORE for the subject with respect to SIRT1 gene product expression that is greater than a pre-determined cut-off value, which in some embodiments can be selected from the group consisting of 1.0, 1.1, 1.2, 1.3, 1.4, 1.5, 1.6, 1.7, 1.8, 1.9, and 2.0. The HSCORE system may be used for BCL6, K-ras, and any other biomarker disclosed herein in the same manner. Endometriosis is the leading cause of IVF failure and is often asymptomatic in 20 to 30% of cases. Endometriosis through inflammatory changes, causes progesterone resistance. Our understanding of the mechanisms involved in endometriosis-related implantation failure has expanded rapidly in recent years. We reported that Sirtuin-1 (SIRT1) a histone deacetylase induced by Kras, is elevated in the endometrium of women with endometriosis. This enzyme targets many of the critical genes required for normal progesterone action and implantation. Researchers have shown that histone deacetylases and the epigenetic changes related to their expression are valuable therapeutic targets. The availability of a specific SIRT1 inhibitor that is safe in human volunteers, provides a new and effective alternative to 2 to 3 months of GnRHa/letrozole therapy with the associated delays in treatment and severe side effects. By inhibiting the underlying cause of progesterone resistance prior to transfer of embryos, the adverse effects of aberrant SIRT1 expression can be avoided. SIRT1 activity is uniquely positioned as a therapeutic target, since SIRT1 is normally only expressed during menses in normal women. In endometriosis cases, SIRT1 is expressed throughout the menstrual cycle. Animal studies in mice demonstrate that SIRT1 over-expression renders the mice infertile. Endometriosis leads to aberrant expression of SIRT1 in mice. When Ex-527 is administered to SIRT1 over-expressing mice, normal implantation is restored. The number and size of endometriotic implants increases in SIRT1-overexpressing mice, and lessens after EX-527 treatment. In some embodiments, EX-527 may be administered in non-pregnant human females for 5 days before embryo implantation. The drug will provide an efficient way to block the anti-progesterone actions of SIRT1 interfering with implantation and resulting in infertility and pregnancy loss. Data from normal volunteers demonstrates that side effects are minimal; evidence from the CDC suggests this drug could benefit over 50,000 women per year who currently fail IVF. The majority of women failing IVF now appear to exhibit progesterone resistance that is often associated with undiagnosed endometriosis. In some embodiments, the treatment comprises administering an effective amount of an SIRT1 inhibitor to the subject. SIRT1 inhibitors include, but are not limited to anti-SIRT1 antibodies, small molecules (see e.g., U.S. Patent Application Publication No.2009/0022694; PCT International Patent Application Publication No. WO 2010/090830; U.S. Patent Application Publication No.2013/0338178) such as but not limited to 1,2-dihydro-3H- naphtho[2,1-b]pyran-3-one (splitomicin; available from Sigma-Aldrich Corp., St. Louis, Missouri), cyclic lipopeptide surfactin and derivatives thereof (see e.g., Chakrabarty et al., 2008), and microRNAs, such as but not limited to those disclosed in, for example, Yamakuchi et al., 2008; Gambari et al., 2011; Xu et al., 2011), which in some embodiments can be miR-34a, miR-22, or a derivative thereof. In some embodiments, the SIRT1 inhibitor may be E-527 Selisistat (EX-527; Racemic 6-chloro-2,3,4,9-terahydro-1H carbazole-1-caboxamide) is a first-in-class specific SIRT1 inhibitor. SIRT1 in a multifunctional histone deacetylase that promotes cellular longevity and proliferation. It appears in the body associated with inflammation and is widely expressed in malignancies. This SIRT1 inhibitor has been studied in Huntington's disease where SIRT1 over-expression has been described. In healthy volunteers, Selisistat was found to be well-tolerated and rapidly absorbed using oral route of administration, with systemic exposure increasing related to dose. The incidence of drug related adverse events were not related to dose or number of doses given. It reached steady state levels in 4 days and had a half-life of 6 hours at the highest dose (600 mg). Expected transcription changes were noted in peripheral blood, consistent with it function as a histone deacetylase. In doses up to 600 mg, there were no findings of physical or neurological exam in volunteers using this drug. The most common adverse reaction was headache, but this was present in placebo group as often as in the treatment group. Selisistat binds to and antagonizes the enzymatic activity of the SIRT1 enzyme. It is one of a class of low-molecular weight, cell permeable, orally bioavailable and metabolically stable compounds previously described. Kinetic analyses suggest this compound binds after the release of nicotinamide from the enzyme and prevents the release of deacetylated peptide and O-acetyl-ADP-ribose, the products of the enzyme-catalyzed deacetylation. Multiple studies have been performed using this compound (EX-527) with activities for reducing inflammation associated with rheumatoid arthritis, T-cell function, protection of ischemic injury after myocardial infarction and hepatic damage, among others. SIRT1 is induced in many circumstances including through inflammation and Kras and resveratrol. In endometrium of women with endometriosis, SIRT1 is aberrantly expressed. SIRT1 appears to be highly expressed at the time of menses in normal women; by blocking the actions of progesterone and inducing progesterone resistance, SIRT1 may facilitate the transition between the secretory and proliferative phases of the menstrual cycle. The over-expression of SIRT1 during the time of implantation in endometriosis, helps explain why menstrual proteins including matrix-metalloproteinases, Cox-2, amphiregulin, and others are aberrantly expressed at the time of implantation in women with this disease. SIRT1 inhibitor (Selisistat) will provide a novel therapy to blunt the effect of aberrant SIRT1 expression associated with infertility and pregnancy loss, and will improve IVF outcomes including live birth rate and reduced miscarriage rate similar to what we demonstrated with GnRH agonist therapy; or Letrozole. Endometriosis is associated with dramatic elevations in SIRT1 and Kras. Selisistat (EX-527) is a selective SIRT1 inhibitor (IC5038 nM) identified from a high throughput screen. EX-527 is more selective for SIRT1 that for SIRT2 or SIRT3 (200-500 fold). EX-527 passed phase I and II studies for therapy of Huntington's disease (NCT01485952, NCT01485965, NCT01521585, NCT01521832; data from http://clinicaltrials.gov). In a separate clinical trial EX-527 was found to be safe and well tolerated in doses up to a maximum dose of 600 mg, and repeated doses of 300 mg/day for up to 7 days in healthy volunteers. Resveratrol, a potent stimulator of SIRT1, was recently shown to be detrimental to embryo implantation in the setting of IVF. Down-regulation of endometriosis reduces inflammation and improves IVF outcomes. Inflammation through KRAS drives SIRT1 expression. SIRTl has been shown to down-regulate at critical genes regulating endometrial receptivity and progesterone action. The actions of SIRTl curtail progesterone action, and likely blocks progesterone responses at the time of menses, to facilitate the transition between the secretory phase and the beginning of a new proliferative phase in non-conception cycles. Endometriosis is one example of an inflammatory condition associated with progesterone resistance acting through KRAS, that stimulates premature and aberrant expression of SIRTI during the time of embryo implantation. By inducing SIRTl, a receptive endometrium is transformed into a menstrual-like non-receptive endometrium, preventing timely embryo attachment and successful pregnancy. By blocking this aberrant, premature expression of SIRTI, progesterone resistance can be avoided and down-stream gene expression of progesterone-regulated genes required for implantation will be expressed. It is contemplated herein that may be carried out in normal volunteers with endometriosis to determine the optimal time of exposure and minimal dose required to restore normal endometrial receptivity. Once an effective dose is established, Phase III clinical trials of this drug are envisioned (SAFER Trial; NCT 04184323). In some embodiments, the treatment may optionally comprise administering an effective amount of a BCL6 inhibitor to the subject, either alone or as part of a combination treatment with an SIRT1 inhibitor. Exemplary BCL6 inhibitors include small molecules (see. e.g., U.S. Patent No.8,338,464; U.S. Patent Application Publication No.2012/0014979 (see e.g., compounds of Formula I described therein, particularly molecule 79-6 (2-[5-(5-bromo-2- oxo-1,2-dihydro-indole-3-ylidene)-4-oxo-2-thiazolidin-3-yl]-succinic acid)); PCT International Patent Application Publication No. WO 2014/204859); peptides and peptidomimetics, such as but not limited to the "BCL6 Peptide Inhibitors ("BPIs"); see U.S. Patent No.8,791,075); the BCL6 inhibitor peptide described in U.S. Patent No.8,841,414 and Polo et al., 2004); anti-BCL6 antibodies and fragments and derivatives thereof; etc. Thus, one aspect of the present invention comprises a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a BCL6 gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject and also has a level of expression of the BCL6 gene product that is greater than the level of expression of the BCL6 gene product of the control subject; and g) administering to the subject an effective amount of EX- 527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) detecting a level of expression of a BCL6 gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product detected in (d); f) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject obtained and an HSCORE calculated for a level of expression of a BCL6 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. In some embodiments, the pre-determined cut-off value is selected from the group consisting of 1.0, 1.1, 1.2, 1.3, 1.4, 1.5, 1.6, 1.7, 1.8, 1.9, and 2.0. Another aspect of the present invention provides a method for increasing the likelihood of implantation of an embryo in a subject, optionally in a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene product and a BCL6 gene product, comprising administering to the subject having overexpression of a SIRT1 gene product and a BCL6 gene product an effective amount of EX-527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method of treating infertility in a subject in need thereof, comprising administering to a subject, optionally a subject having overexpression of a SIRT1 gene product and a BCL6 gene product, an effective amount of EX-527, optionally in combination with a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity. Another aspect of the present invention provides a method of treating endometriosis in a subject in need thereof, comprising administering to a subject, optionally a subject having overexpression of a SIRT1 gene product and a BCL6 gene product, an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a BCL6 gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and has a level of expression of the BCL6 gene product that is greater than the level of expression of the BCL6 gene product of the control subject; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) detecting a level of expression of a BCL6 gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression detected in (d); f) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject an HSCORE calculated for the level of expression of a BCL6 gene product that is greater than a pre-determined cut-off value; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a BCL6 gene product in a sample of endometrium obtained from a control subject during the second half of said control subject’s menstrual cycle; f) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and a level of expression of the BCL6 gene product greater than the level of expression of the BCL6 gene product of the control subject; g) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a BCL6 gene product in the subsequent sample; and k) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (i) and comparing the level of expression of the BCL6 gene product detected in (c) with the level of expression of the BCL6 gene product detected in (j), wherein a decrease in (i) relative to (b) and a decrease in (j) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (i) relative to (b) and an increase or no change in (j) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a BCL6 gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the first sample; f) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value and an HSCORE based on the level of expression of the BCL6 gene product that is greater than a pre-determined cut-off level; g) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; k) detecting a level of expression of a BCL6 gene product in the subsequent sample; l) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the subsequent sample; and m) comparing the HSCORE of (c) with the HSCORE of (j) and comparing the HSCORE of (e) with the HSCORE of (l), wherein a decrease in the HSCORE of (j), along with a decrease in the HSCORE of (l) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (j) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (l) indicates that treatment of the endometriosis and/or infertility can be continued or increased. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject and also has a level of expression of the K-ras gene product that is greater than the level of expression of the K-ras gene product of the control subject; and g) administering to the subject an effective amount of EX- 527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) detecting a level of expression of a K-ras gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product detected in (d); f) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject obtained and an HSCORE calculated for a level of expression of a K-ras gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method for increasing the likelihood of implantation of an embryo in a subject, optionally a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene product and a K-ras gene product, comprising administering to the subject (e.g., the subject having overexpression of a SIRT1 gene product and a K-ras gene product) an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of treating infertility in a subject in need thereof, comprising administering to a subject, optionally a subject having overexpression of a SIRT1 gene product and a K-ras gene product, an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of treating endometriosis in a subject in need thereof, comprising administering to a subject, optionally a subject having overexpression of a SIRT1 gene product and a K-ras gene product, an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and has a level of expression of the K-ras gene product that is greater than the level of expression of the K- ras gene product of the control subject; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) detecting a level of expression of a K-ras gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression detected in (d); f) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject an HSCORE calculated for the level of expression of a K-ras gene product that is greater than a pre-determined cut-off value; and g) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject during the second half of said control subject’s menstrual cycle; f) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and a level of expression of the K-ras gene product greater than the level of expression of the K-ras gene product of the control subject; g) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a K-ras gene product in the subsequent sample; and k) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (i) and comparing the level of expression of the K-ras gene product detected in (c) with the level of expression of the K-ras gene product detected in (j), wherein a decrease in (i) relative to (b) and a decrease in (j) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (i) relative to (b) and an increase or no change in (j) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a K-ras gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the first sample; f) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value and an HSCORE based on the level of expression of the K-ras gene product that is greater than a pre-determined cut-off level; g) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; k) detecting a level of expression of a K-ras gene product in the subsequent sample; l) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the subsequent sample; and m) comparing the HSCORE of (c) with the HSCORE of (j) and comparing the HSCORE of (e) with the HSCORE of (l), wherein a decrease in the HSCORE of (j), along with a decrease in the HSCORE of (l) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (j) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (l) indicates that treatment of the endometriosis and/or infertility can be continued or increased. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin- releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) detecting a level of expression of a K-ras gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f) and comparing the level of expression of the K-ras gene product detected in (c) with the level of expression of the K-ras gene product detected in (g), wherein a decrease in (f) relative to (b) and a decrease in (g) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) and an increase or no change in (g) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a K-ras gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the first sample; f) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; g) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (f); h) detecting a level of expression of a SIRT1 gene product in the subsequent sample; i) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a K-ras gene product in the subsequent sample; k) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the subsequent sample; and l) comparing the HSCORE of (c) with the HSCORE of (i) and comparing the HSCORE of (e) with the HSCORE of (k), wherein a decrease in the HSCORE of (i), along with a decrease in the HSCORE of (k) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (i) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (k) indicates that treatment of the endometriosis and/or infertility can be continued or increased. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a BCL6 gene product in the sample; d) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with an effective amount of a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) detecting a level of expression of a BCL6 gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f) and comparing the level of expression of the BCL6 gene product detected in (c) with the level of expression of the BCL6 gene product detected in (g), wherein a decrease in (f) relative to (b) and a decrease in (g) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) and an increase or no change in (g) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a BCL6 gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the first sample; f) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of a BCL6 inhibitor and/or a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; g) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (f); h) detecting a level of expression of a SIRT1 gene product in the subsequent sample; i) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a BCL6 gene product in the subsequent sample; k) calculating an HSCORE for the subject based on the level of expression of the BCL6 gene product in the subsequent sample; and l) comparing the HSCORE of (c) with the HSCORE of (i) and comparing the HSCORE of (e) with the HSCORE of (k), wherein a decrease in the HSCORE of (i), along with a decrease in the HSCORE of (k) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (i) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (k) indicates that treatment of the endometriosis and/or infertility can be continued or increased. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject; f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject and also has a level of expression of the K-ras gene product that is greater than the level of expression of the K-ras gene product of the control subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K-ras inhibitor and/or a treatment that blocks or reduces K-ras activity. Another aspect of the present invention provides a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) detecting a level of expression of a K-ras gene product in the sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product detected in (d); f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject obtained and an HSCORE calculated for a level of expression of a K-ras gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of a K- ras inhibitor and/or a treatment that blocks or reduces K-ras activity. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the present invention provides a method of treating endometriosis derived ovarian cancer in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product and a K-ras gene product an effective amount of EX-527, optionally in combination with a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the present invention provides a method of managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) detecting a level of expression of a K-ras gene product in the sample; d) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; e) comparing the level of expression detected in (c) with the level of expression of a K-ras gene product in a sample of endometrium obtained from a control subject during the second half of said control subject’s menstrual cycle; f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject, and a level of expression of the K-ras gene product greater than the level of expression of the K-ras gene product of the control subject; g) treating the endometriosis derived ovarian cancer by administering to the subject an effective amount of EX-527, optionally in combination with a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) detecting a level of expression of a K-ras gene product in the subsequent sample; and k) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (i) and comparing the level of expression of the K-ras gene product detected in (c) with the level of expression of the K-ras gene product detected in (j), wherein a decrease in (i) relative to (b) and a decrease in (j) relative to (c) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (i) relative to (b) and an increase or no change in (j) relative to (c) indicates that the treatment can be continued or increased. Another aspect of the present invention provides a method for managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) detecting a level of expression of a K-ras gene product in the first sample; e) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the first sample; f) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value and an HSCORE based on the level of expression of the K-ras gene product that is greater than a pre-determined cut-off level; g) treating the endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with a K- ras inhibitor, a treatment that blocks or reduces K-ras activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; h) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (g); i) detecting a level of expression of a SIRT1 gene product in the subsequent sample; j) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; k) detecting a level of expression of a K-ras gene product in the subsequent sample; l) calculating an HSCORE for the subject based on the level of expression of the K-ras gene product in the subsequent sample; and m) comparing the HSCORE of (c) with the HSCORE of (j) and comparing the HSCORE of (e) with the HSCORE of (l), wherein a decrease in the HSCORE of (j), along with a decrease in the HSCORE of (l) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (j) to a value greater than or equal to a pre-determined cut-off value, along with either no change or an increase in the HSCORE of (l) indicates that treatment of the endometriosis and/or infertility can be continued or increased. In some embodiments, the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. Another aspect of the invention comprises method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre- determined cut-off value, as measured in a sample of endometrium from the subject obtained; and e) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method for increasing the likelihood of implantation of an embryo in a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene, comprising administering to the subject having overexpression of a SIRT1 gene an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of treating infertility in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of treating endometriosis in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and e) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and e) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; d) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and g) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f), wherein a decrease in (f) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value; e) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX- 527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; h) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and i) comparing the HSCORE of (c) with the HSCORE of (h), wherein a decrease in the HSCORE of (h) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (h) to a value greater than or equal to a pre- determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises a method of managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; d) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (c); e) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and f) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (e), wherein a decrease in (e) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (e) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and h) comparing the HSCORE of (c) with the HSCORE of (g), wherein a decrease in the HSCORE of (g) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (g) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises a method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; d) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (c); e) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and f) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (e), wherein a decrease in (e) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (e) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and h) comparing the HSCORE of (c) with the HSCORE of (g), wherein a decrease in the HSCORE of (g) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (g) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. Another aspect of the invention comprises a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and e) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and e) administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity. Another aspect of the invention comprises a method of treating endometriosis derived ovarian cancer in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist. Another aspect of the invention comprises a method of managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject, optionally obtained during the first and/or second half (e.g., secretory phase and/or proliferative phase) of the subject's menstrual cycle; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject, optionally obtained during the first and/or the second half (e.g., secretory phase and/or proliferative phase) of the subject's menstrual cycle; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; e) treating the endometriosis derived ovarian cancer by administering to the subject an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (g), wherein a decrease in (g) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (g) relative to (b) indicates that the treatment can be continued or increased. Another aspect of the invention comprises a method for managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value; e) treating the endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with progesterone and/or a treatment that enhances progesterone activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; h) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and i) comparing the HSCORE of (c) with the HSCORE of (h), wherein a decrease in the HSCORE of (h) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (h) to a value greater than or equal to a pre- determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased. In some embodiments of the methods disclosed herein, the HSCORE may be calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. The presence and/or expression level of each of the presently disclosed biomarkers can be determined in a variety of animal tissues. In some embodiments, the biomarkers can be detected and/or quantified in animal tissue or bodily fluids. In some embodiments, the biomarkers can be detected and/or quantified in tissue. Any suitable method can be employed for determining the presence and/or expression level of each of the biomarkers, as would be apparent to one skilled in the art upon a review of the present disclosure. For example, methods for detecting and/or quantified biomarkers can include, but are not limited to, polymerase chain reaction (PCR)-based techniques, gas chromatography (GC), liquid chromatography/mass spectroscopy (LC-MS), gas chromatography/mass spectroscopy (GC-MS), nuclear magnetic resonance (NMR), magnetic resonance imaging (MRI), Fourier Transform InfraRed (FT-IR), and inductively coupled plasma mass spectrometry (ICP-MS). It is further understood that mass spectrometry techniques include, but are not limited to, the use of magnetic-sector and double focusing instruments, transmission quadrapole instruments, quadrupole ion-trap instruments, time-of- flight instruments (TOF), Fourier transform ion cyclotron resonance instruments (FT-MS), and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI- TOF MS). In some embodiments, protein biomarkers can be detected and/or quantified using technologies well known to those of skill in the art such as gel electrophoresis, immunohistochemistry, and antibody binding. Methods for generating antibodies to a polypeptide of interest (e.g., an SIRT1 peptide or polypeptide, a BCL6 peptide or polypeptide, a k-ras peptide or polypeptide, a progesterone peptide or polypeptide) are well known to those of ordinary skill in the art. An antibody against a protein biomarker of the presently disclosed subject matter can be any monoclonal or polyclonal antibody, so long as it suitably recognizes the protein biomarker. In some embodiments, antibodies are produced using the protein biomarker as the immunogen according to any conventional antibody or antiserum preparation process. The presently disclosed subject matter provides for the use of both monoclonal and polyclonal antibodies. In addition, a protein used herein as the immunogen is not limited to any particular type of immunogen. For example, fragments of the protein biomarkers of the presently disclosed subject matter can be used as immunogens. The fragments can be obtained by any method including, but not limited to, expressing a fragment of the gene encoding the protein, enzymatic processing of the protein, chemical synthesis, and the like. Antibodies against the instantly disclosed biomarkers can also be purchased from commercial suppliers such as, but not limited to Santa Cruz Biotechnology, Inc. (Santa Cruz, California, United States of America), ABCAM® (Cambridge, Massachusetts, United States of America), Cell Signaling Technology, Inc. (Danvers, Massachusetts, United States of America), Thermo Fisher Scientific Inc. (Rockford, Illinois, United States of America), eBioscience, Inc. (San Diego, California, United States of America), etc. The invention will now be described with reference to the following examples. It should be appreciated that these examples are not intended to limit the scope of the claims to the invention but are rather intended to be exemplary of certain embodiments. Any variations in the exemplified methods that occur to the skilled artisan are intended to fall within the scope of the invention. The present invention can be practiced for prophylactic, therapeutic and/or diagnostic purposes. Also provided herein are compositions comprising EX-527 (e.g., an effective amount of EX-527) for use in any of the methods disclosed herein. A composition of the present invention may be administered in any frequency, amount, and/or route as needed to elicit an effective therapeutic effect in a subject (e.g., in a subject in need thereof) as described herein. In certain embodiments, a composition is administered/delivered to the subject, e.g., systemically (e.g., intravenously). In particular embodiments, more than one administration (e.g., two, three, four or more administrations) may be employed to achieve the desired level of dosage over a period of various intervals, e.g., daily, weekly, monthly, yearly, etc. The most suitable route in any given case will depend on the nature and severity of the condition being treated and on the nature of the particular delivery method that is being used. In embodiments wherein a vector is used for delivery, the vector will typically be administered in a liquid formulation by direct injection (e.g., stereotactic injection) to the desired region or tissues. In some embodiments, the vector can be delivered via a reservoir and/or pump. In other embodiments, the vector may be provided by topical application to the desired region or by intra-nasal administration of an aerosol formulation. Administration to the eye or into the ear, may be by topical application of liquid droplets. As a further alternative, the vector may be administered as a solid, slow-release formulation. For example, controlled release of parvovirus and AAV vectors is described in international patent publication WO 01/91803, which is incorporated by reference herein for these teachings. Administration may be by any suitable means, such as intraperitoneally, intramuscularly, intranasally, intravenously, intradermally (e.g., by a gene gun), intrarectally and/or subcutaneously. The compositions herein may be administered via a skin scarification method, and/or transdermally via a patch or liquid. The compositions can be delivered subdermally in the form of a biodegradable material that releases the compositions over a period of time. As further non-limiting examples, the route of administration can be by inhalation (e.g., oral and/or nasal inhalation), oral, buccal (e.g., sublingual), rectal, vaginal, topical (including administration to the airways), intraocular, by parenteral (e.g., intramuscular [e.g., administration to skeletal muscle], intravenous, intra-arterial, intraperitoneal and the like), subcutaneous (including administration into the footpad), intrapleural, intracerebral, intrathecal, intraventricular, intra-aural, intra-ocular (e.g., intra- vitreous, sub-retinal, anterior chamber) and peri-ocular (e.g., sub-Tenon's region) routes or any combination thereof. As another example, delivery can be via a liposome, using commercially available liposome preparations such as LIPOFECTIN, LIPOFECTAMINE (GIBCO-BRL, Inc., Gaithersburg, MD), SUPERFECT (Qiagen, Inc. Hilden, Germany) and TRANSFECTAM (Promega, Madison, WI), as well as other liposomes developed according to procedures standard in the art. In addition, the nucleic acid or vector of this invention can be delivered in vivo by electroporation, the technology for which is available from Genetronics, Inc. (San Diego, CA) as well as by means of a SONOPORATION machine (ImaRx Pharmaceutical Corp., Tucson, AZ). The present invention further provides a kit comprising one or more compositions of this invention. It would be well understood by one of ordinary skill in the art that the kit of this invention can comprise one or more containers and/or receptacles to hold the reagents (e.g., EX-527 and/or other agonists or antagonists disclosed herein) of the kit, along with appropriate buffers and/or diluents and/or other solutions and directions for using the kit, as would be well known in the art. Such kits can further comprise adjuvants and/or other immunostimulatory or immunomodulating agents, as are well known in the art. The compositions and kits of the present invention can also include other medicinal agents, pharmaceutical agents, carriers, diluents, immunostimulatory cytokines, etc. Actual methods of preparing such dosage forms are known, or will be apparent, to those skilled in this art. The pharmaceutical formulations of the invention can optionally comprise other medicinal agents, pharmaceutical agents, stabilizing agents, buffers, carriers, diluents, salts, tonicity adjusting agents, wetting agents, and the like, for example, sodium acetate, sodium lactate, sodium chloride, potassium chloride, calcium chloride, sorbitan monolaurate, triethanolamine oleate, etc. For injection, the carrier will typically be a liquid. For other methods of administration, the carrier may be either solid or liquid. For inhalation administration, the carrier will be respirable, and is typically in a solid or liquid particulate form. The pharmaceutical formulations can be packaged for use as is, or lyophilized, the lyophilized preparation generally being combined with a sterile aqueous solution prior to administration. The compositions can further be packaged in unit/dose or multi-dose containers, for example, in sealed ampoules and vials. The pharmaceutical formulations can be formulated for administration by any method known in the art according to conventional techniques of pharmacy. For example, the compositions can be formulated to be administered intranasally, by inhalation (e.g., oral inhalation), orally, buccally (e.g., sublingually), rectally, vaginally, topically, intrathecally, intraocularly, transdermally, by parenteral administration (e.g., intramuscular [e.g., skeletal muscle], intravenous, subcutaneous, intradermal, intrapleural, intracerebral and intra-arterial, intrathecal), or topically (e.g., to both skin and mucosal surfaces, including airway surfaces). For intranasal or inhalation administration, the pharmaceutical formulation can be formulated as an aerosol (this term including both liquid and dry powder aerosols). For example, the pharmaceutical formulation can be provided in a finely divided form along with a surfactant and propellant. Typical percentages of the composition are 0.01-20% by weight, preferably 1-10%. The surfactant is generally nontoxic and soluble in the propellant. Representative of such agents are the esters or partial esters of fatty acids containing from 6 to 22 carbon atoms, such as caproic, octanoic, lauric, palmitic, stearic, linoleic, linolenic, olesteric and oleic acids with an aliphatic polyhydric alcohol or its cyclic anhydride. Mixed esters, such as mixed or natural glycerides may be employed. The surfactant may constitute 0.1-20% by weight of the composition, preferably 0.25-5%. The balance of the composition is ordinarily propellant. A carrier can also be included, if desired, as with lecithin for intranasal delivery. Aerosols of liquid particles can be produced by any suitable means, such as with a pressure-driven aerosol nebulizer or an ultrasonic nebulizer, as is known to those of skill in the art. See, e.g., U.S. Patent No.4,501,729. Aerosols of solid particles can likewise be produced with any solid particulate medicament aerosol generator, by techniques known in the pharmaceutical art. Intranasal administration can also be by droplet administration to a nasal surface. Injectable formulations can be prepared in conventional forms, either as liquid solutions or suspensions, solid forms suitable for solution or suspension in liquid prior to injection, or as emulsions. Alternatively, one can administer the pharmaceutical formulations in a local rather than systemic manner, for example, in a depot or sustained-release formulation. Extemporaneous injection solutions and suspensions can be prepared from sterile powders, granules and tablets of the kind previously described. For example, an injectable, stable, sterile formulation of the invention in a unit dosage form in a sealed container can be provided. The formulation can be provided in the form of a lyophilizate, which can be reconstituted with a suitable pharmaceutically acceptable carrier to form a liquid composition suitable for injection into a subject. The unit dosage form can be from about 1 µg to about 10 grams of the formulation. When the formulation is substantially water-insoluble, a sufficient amount of emulsifying agent, which is pharmaceutically acceptable, can be included in sufficient quantity to emulsify the formulation in an aqueous carrier. One such useful emulsifying agent is phosphatidyl choline. Pharmaceutical formulations suitable for oral administration can be presented in discrete units, such as capsules, cachets, lozenges, or tables, as a powder or granules; as a solution or a suspension in an aqueous or non-aqueous liquid; or as an oil-in-water or water- in-oil emulsion. Oral delivery can be performed by complexing a compound(s) of the present invention to a carrier capable of withstanding degradation by digestive enzymes in the gut of an animal. Examples of such carriers include plastic capsules or tablets, as known in the art. Such formulations are prepared by any suitable method of pharmacy, which includes the step of bringing into association the protein(s) and a suitable carrier (which may contain one or more accessory ingredients as noted above). In general, the pharmaceutical formulations are prepared by uniformly and intimately admixing the compound(s) with a liquid or finely divided solid carrier, or both, and then, if necessary, shaping the resulting mixture. For example, a tablet can be prepared by compressing or molding a powder or granules, optionally with one or more accessory ingredients. Compressed tablets are prepared by compressing, in a suitable machine, the formulation in a free-flowing form, such as a powder or granules optionally mixed with a binder, lubricant, inert diluent, and/or surface active/dispersing agent(s). Molded tablets are made by molding, in a suitable machine, the powdered protein moistened with an inert liquid binder. Pharmaceutical formulations suitable for buccal (sub-lingual) administration include lozenges comprising the compound(s) in a flavored base, usually sucrose and acacia or tragacanth; and pastilles in an inert base such as gelatin and glycerin or sucrose and acacia. Pharmaceutical formulations suitable for parenteral administration can comprise sterile aqueous and non-aqueous injection solutions, which preparations are preferably isotonic with the blood of the intended recipient. These preparations can contain anti- oxidants, buffers, bacteriostats and solutes, which render the composition isotonic with the blood of the intended recipient. Aqueous and non-aqueous sterile suspensions, solutions and emulsions can include suspending agents and thickening agents. Examples of nonaqueous solvents are propylene glycol, polyethylene glycol, vegetable oils such as olive oil, and injectable organic esters such as ethyl oleate. Aqueous carriers include water, alcoholic/aqueous solutions, emulsions or suspensions, including saline and buffered media. Parenteral vehicles include sodium chloride solution, Ringer's dextrose, dextrose and sodium chloride, lactated Ringer's, or fixed oils. Intravenous vehicles include fluid and nutrient replenishers, electrolyte replenishers (such as those based on Ringer's dextrose), and the like. Preservatives and other additives may also be present such as, for example, antimicrobials, anti-oxidants, chelating agents, and inert gases and the like. Pharmaceutical formulations suitable for rectal administration are optionally presented as unit dose suppositories. These can be prepared by admixing the active agent with one or more conventional solid carriers, such as for example, cocoa butter and then shaping the resulting mixture. Pharmaceutical formulations suitable for topical application to the skin preferably take the form of an ointment, cream, lotion, paste, gel, spray, aerosol, or oil. Carriers that can be used include, but are not limited to, petroleum jelly, lanoline, polyethylene glycols, alcohols, transdermal enhancers, and combinations of two or more thereof. In some embodiments, for example, topical delivery can be performed by mixing a pharmaceutical formulation of the present invention with a lipophilic reagent (e.g., DMSO) that is capable of passing into the skin. Pharmaceutical formulations suitable for transdermal administration can be in the form of discrete patches adapted to remain in intimate contact with the epidermis of the subject for a prolonged period of time. Formulations suitable for transdermal administration can also be delivered by iontophoresis (see, for example, Pharmaceutical Research 3:318 (1986)) and typically take the form of a buffered aqueous solution of the compound(s). Suitable formulations can comprise citrate or bis\tris buffer (pH 6) or ethanol/water and can contain from 0.1 to 0.2M active ingredient. EXAMPLES Example 1: Endometrial biopsies were obtained at the time of surgery from regularly cycling women between the ages of 18 and 45. Use of an intrauterine device or hormonal therapies in the 3 months preceding surgery was exclusionary for this study. Control samples were obtained from 39 women without infertility or suspected endometriosis collected from the proliferative (n = 7), secretory phases (n = 23), and menses (n = 9). Endometriosis affected eutopic endometrium samples from 39 women were collected from the proliferative (n = 14) and secretory phases (n = 25). Endometrial biopsies were either obtained in luteinizing hormone–timed natural cycles prior to laparoscopy or at the time of laparoscopy for endometriosis. Stage of endometriosis was based on the American Society for Reproductive Medicine classification criteria and recorded as minimal or mild (Stage I or II) or moderate to severe (Stage III or IV). Written consent was obtained for collection of endometrial biopsies from normal controls and women with infertility and demonstrated endometriosis. All specimens were deidentified prior to use. Baseline characteristics of the study population were as follows. Control: Age range 20-49, mean 34.82. Endometriosis: Age range 25-42, mean 32.7; Stage of disease (number of participants): I (14), II (20), III (17), IV (3). Animals and tissue collection: For the uteri samples during early pregnancy, wild-type female mice at 8 weeks of age were individually mated with wild-type male mice, and uteri were collected at different time points of pregnancy. The initiation of pregnancy was marked by the presence of the postcoital vaginal plug at gestation day (GD) 0.5 for the early pregnancy study. Uterine tissues were flash frozen at the time of collection for RNA isolation or fixed with 4% paraformaldehyde (vol/vol) and paraffin embedded for immunostaining analysis. Sirt1 conditional overexpressed mice were generated by crossing Pgrcre/+ (31) with Rosa26Sirt1 (32) mice (Pgr cre/+Rosa26Sirt1; Sirt1Over). To assess the effect of SIRT1 overexpression on female reproductive ability, 8-week-old Sirt1Over mice and control female mice were individually mated to fertile wild-type male mice (n = 4). The numbers of litters and pups were recorded from each female mouse. For artificial decidualization, 6-week-old control and Sirt1^Over female mice (n = 5 per genotype) were ovariectomized. After 2 weeks rest, the mice were treated daily with subcutaneous injections (s.c.) of E2 (100 ng) for 3 days. The mice were treated daily with 1 mg of P s.c. and 6.7 ng of E2 s.c. for 3 days after undergoing 2 days of rest. The left horn of each mouse was mechanically scratched the full length of the anti-mesometrial lumen 6 h after the third P and E2 injection, while the right horn was left unstimulated as an adjusted control. To induce the maximal decidual reaction, the mice continued daily treatment with s.c. injections of 1 mg P and 6.7 ng E2 for 5 days after the mechanical stimulation. Uterine tissues were collected, and then weights were measured from both horns. Uterine tissues were flash frozen for RNA isolation or fixed with 4% paraformaldehyde (vol/vol) and paraffin embedded for histological analysis. Menstrual mouse model was induced as previous reported (Xu et al.2007 Hum Reprod. 22(12):3184-3191). Briefly, after induction of artificial decidualization, hormone injection was withdrawn for 24 h after 5-day injection from mechanical stimulation. For immunohistochemistry (IHC) analyses, uterine sections were exposed to anti- SIRT1 (CS-9475S, Cell Signaling, Danvers, MA, USA; RRID AB_2617130), progesterone receptor (PGR; CS-8757S, Cell Signaling; RRID AB_2797144), and anti- Ki67 (BD550609, BD Bioscience, San Jose, CA, USA; RRID AB_393778). The sections were then exposed to antirabbit or antimouse secondary antibody solution (Vector Laboratories, Burlingame, CA, USA) and then incubated in horseradish peroxidase (ThermoFisher Scientific, Waltham, MA, USA). The signal was detected by the Vectastain Elite DAB kit (Vector Laboratories). To compare the IHC staining intensities, a semiquantitative grade (HSCORE) was calculated by adding the percentage of strongly stained nuclei (3×), the percentage of moderately stained nuclei (2×), and the percentage of weakly stained nuclei (1×) in a region of approximately 100 cells, giving a possible range of 0 to 300 (35). RNA isolation and quantitative real-time polymerase chain reaction (RT-qPCR): Total RNA was isolated from the uteri using a Qiagen RNeasy total RNA isolation kit (Qiagen). The expression of Sirt1, Muc-1, Clca3, Ltf, Fst, Klf15, Patch1, and Gli was quantified by RT-qPCR analysis using an Applied Biosystems StepOnePlus system according to manufacturer instructions (Applied Biosystem). Template complementary DNA was generated from 1 µg of total RNA using random hexamers and MMLV Reverse Transcriptase (Invitrogen Corp). Standard curves were produced by serial dilution of a prepared sample of total RNA isolated from the mouse uteri. The results of RT-qPCR were normalized by Rpl7 RNA using an SYBR Green master mix reagent. For immunoprecipitation experiments, Ishikawa cells were transfected with SIRT1, progesterone receptor (PR)-A, and PR-B. Five hundred micrograms of lysates were immunoprecipitated with 1 μg of anti-SIRT1 antibodies (CS-9475S, Cell Signaling) with 30 μL of resuspended protein A-agarose (Pierce Biotechnology, Rockford, IL, USA) and incubated overnight at 4°C. Immunocomplexes were subjected via sodium dodecyl sulfate- polyacrylamide gel electrophoresis and transferred onto polyvinylidene difluoride membrane (Millipore, Bedford, MA, USA). The membrane was exposed to anti-SIRT1 or anti- progesterone receptor (PGR) (CS-8757S, Cell Signaling) antibodies. After the incubation with a horseradish peroxidase-linked secondary antibody, immunoreactivity was visualized with enhanced chemiluminescence reagents (GE Healthcare, Pittsburgh, PA, USA). Endometriosis was surgically induced in control (Pgrcre/+R osa26mTmG/+) and Pgrcre/+Rosa26Sirt1/mTmG (Sirt1overRosa26 mTmG) mice by inoculating autologous endometrial tissue into the peritoneal cavity. Briefly, mice were treated with estradiol (100 ng/mouse) for 3 days to synchronize the endometrial growth before endometriosis induction. Under anesthesia, a midline abdominal incision was made to expose the uterus in female mice, and 1 of the uterine horns was removed. In a Petri dish containing phosphate-buffered saline (pH 7.5), the uterine horn was opened longitudinally with scissors. The excised uterine horn was cut into small fragments of about 1 mm³ and then injected back into the peritoneum of the same mouse. The abdominal incision and wound were closed with sutures and skin was closed with surgical wound clips, respectively. The sham group was Pgr^cre/+Rosa26^mTmG/+ mice injected with phosphate-buffered saline without endometrium to rule out the impact of the surgery itself in producing adhesions. One month after endometriosis induction, mG + endometriotic lesions in the mouse were removed and counted under a fluorescence- dissecting microscope. For the EX-527 treatment, the mice with endometriotic lesions were treated with daily administration of vehicle or 0.5 mg/kg EX-527 for 2 weeks. EX-527 at dose of 2.5mg/kg EX-527 is administered to the mice at GD 3.5 and then collected at GD 7.5. We examined SIRT1 expression in mice with experimentally induced endometriosis and showed that SIRT1 was over-expressed by 3 months after which time the mice became infertile. Mice with sham surgery remained fertile. Artificially over-expressing SIRT1 in genetically modified mice resulted in infertility. Treatment with SIRT1 inhibitor EX-527 in these mice restored normal fertility and reduced the size and number of endometriotic implants. These results demonstrate that SIRT1 is directly related to the presence of endometriosis and SIRT1 actively participates in its growth and activity of lesions likely through progesterone resistance. Endometriosis leads to implantation failure that is reversible by administering EX-527. Endometriosis can be surgically induced in Pgrcre/+Rosa26Luc/mTmG mice (luciferase expression in uterine tissues) by inoculating autologous or syngeneic (from litter mate) endometrial tissue into the peritoneal cavity. After one month of endometriosis induction, endometriosis was detected in live animal by bioluminescent imaging and endometriotic lesions were GFP positive. There was no difference between autologous or syngeneic transplant. Our mouse model of endometriosis was developed in Pgrcre/+Rosa26Luc/mTmG mice without ovariectomy and unopposed E2 treatment that produce endometriotic lesions highly similar to those in humans. Our model closely mirrors the human condition as an E2-dependent and P4-suppressed disorder. Bioluminescence imaging offers non-invasive imaging to monitor endometriosis development and progression in living animals.3D in vivo imaging provides exact number and locations of endometriotic lesions in our endometriosis mouse model. mTmG reporter is also useful to isolate pure GFP- positive endometriotic cells for molecular analysis in mice. The Pgrcre/+Rosa26Luc/mTmG mouse is an innovative model for endometriosis etiological studies and quantifying endometriosis lesions. The experiments of this study are further described below. FIG.1 shows histology (panel A) and a bar graph (panel B) of inhibition of endometriosis development by EX-527 in the mouse model described herein. FIG.2 shows representative images of GD5.5 Pgr^cre/+ Sirt1-LSL mice that conditionally over-express SIRT in the uterus. These mice are infertile and display a profound implantation defect (upper images). When those mice are treated with EX-527 (50 ug/mouse) implantation is restored (lower images). SIRT1 and Progesterone (P4) Resistance and Endometriosis: Implications for Infertility Management: Objective: Progesterone (P4) resistance is now considered a central element in endometriosis pathology, but the mechanism and role of P4 resistance in normal uterine function is not understood. SIRT1, an epigenetic regulator that targets key P4-regulated genes, is normally expressed at menses in fertile women and at the time of implantation in mice. In inflammatory pathologic conditions such as endometriosis, SIRT1 is over-expressed at all stages of the menstrual cycle. We hypothesize that SIRT1 is a central regulator of P4- resistance with a role in both normal and abnormal uterine physiology. Design and Methods: SIRT1 was histologically examined in normal implantation sites in mice during early pregnancy. To investigate the role of SIRT1 in endometrial function and endometriosis, we generated uterine specific Sirt1 knock-out (Pgr^cre/+Sirt1^f/f; Sirt1^d/d) and overexpression (Pgr^cre/+ROSA26^LSL-Sirt1 ; Sirt1^Over) mice.2) The effect of SIRT1 on female fertility was examined in Sirt1^d/d mice.3) To assess the effect of SIRT1 overexpression on endometriosis, we surgically induced endometriosis in mice using endometrium from Sirt1^Over and control mice.4) Treatment with SIRT1 inhibitor EX-527 was examined in implantation defects in Sirt1^Over mice. 5) Human endometrium from throughout the cycle including menses were immunostained for SIRT1 in control and endometriosis cases. Results: IHC was performed to examine the expression of SIRT1 in the mouse uterus during early pregnancy. The expression of SIRT1 proteins in the mouse uterus were also weakly detected at the luminal epithelium, glandular epithelium, and stromal cells at GD 2.5 and 3.5 (n = 3/time point) (FIG.3A). To determine whether SIRT1 overexpression is induced after menstruation, we used a mouse model that mimics menstruation-like processes. Decidualization was artificially induced in ovariectomized mice by mechanically scratch. After P withdrawal, endometrial breakdown was observed. SIRT1 proteins were strongly expressed at the menstrual like tissues of mouse (n = 3). The level of SIRT1 proteins was significantly higher in the menstrual like tissues compared to GD 2.5 and GD 3.5 (FIG.3A). SIRT1 was expressed in the decidua of pregnant mice only on the day of implantation, day 5.5 (FIG.3B). Uterine specific Sirt1 knock-out mice were subfertile. Uterine-specific Sirt1 overexpression caused subfertility due to implantation failure and decidualization defects. SIRT1 levels are significantly higher in the eutopic endometrium from endometriosis patients as well as nonhuman primate and rodent animal models. To effectively investigate the effects of Sirt1 overexpression in the endo- metrium, mice with loxP-Stop-loxP-Sirt1 were bred to the Pgr^Cre mouse (Pgr^cre/+Rosa26^Sirt1; Sirt1^over mouse). PGR and Cre activity initially emerge in the luminal and glandular epithelial cell lineages of 2-week-old Pgr^cre/+ mice. At this stage of early development, minimal expression of PGR and Cre was detected in the stroma and myometrium. As the animal sexually matured, Cre activity was not only detected in the luminal and glandular epithelial compartments but also in the stroma and myometrium. Therefore, overexpression of Sirt1 in the uterus was confirmed at GD 3.5 by RT-qPCR (FIG.5B panel A) and immunohistochemical analyses (n = 5/genotype) (FIG.4 panel A). Sirt1 messenger RNAs were significantly increased in uteri of Sirt1^over mice compared to control mice. Although PGR and Cre proteins are expressed in nearly 100% of endometrial epithelial cells at GD 3.5, there are cells negative for PGR and Cre in endometrial stromal cells. In addition, PGR and Cre proteins are not expressed in immune cells or endothelial cells. Our results of SIRT1 IHC revealed that SIRT1 overexpression was validated in 100% of endometrial epithelial cells and 82.9% ± 2.92% of stromal cells in Sirt1over mice (FIG.4 panel A). These results confirm successful overexpression of Sirt1 in the uterus of Sirt1over mice. In the endometriosis mouse model, SIRT1 over-expressing mice have a significantly increased incidence of endometriotic lesions compared to control mice (FIG.4 panels B and C). Infertile SIRT1 over-expressing mice could be rescued with the SIRT1 inhibitor, EX- 527 (FIG.5A). FIG.5B panels A-D provide additional data from these experiments, where in order to assess overall fecundity, control and Sirt1over females were housed with wild- type male mice in a 6-month fertility trial. For control mice, 4 mice were tested, which combined had 21 litters totaling 131 pups, with an average of 6.24 +/- 0.28 pups/litter (mean+/- SEM) and an average of 5.25 +/- 0.17 litters/mouse (mean +/- SEM). For Sirt1^over mice, 4 mice were tested, which combined had 8 litters totaling 27 pups, with an average of 3.38 +/- 0.70 pups/litter (mean+/- SEM) and an average of 2.00 +/- 0.00 litters/mouse (mean +/- SEM). Both groups of mice engaged in normal mating activity resulting in the observation of copulatory plugs. Control mice had 6.24 ± 0.28 pups/litter and 5.25 ± 0.17 litter/mouse, whereas Sirt1over mice had 3.38 ± 0.70 pups/ litter and 2.00 ± 0.00 litter/mouse. Sirt1^over females produced significantly fewer pups per mouse (P < 0.001), fewer litters per mouse (P < 0.001), and fewer pups per litter (P < 0.01) than the control females (n = 4/genotype). Although Cre recombinase expression was reported within the pituitary, ovary, uterus, and mammary gland of the Pgrcre/+ mouse, female Sirt1^over mice showed a normal estrous cycle and ovarian morphology. These results suggest that the fertility defect is primarily due to a uterine defect. Accordingly, to investigate whether SIRT1 overexpression results implantation failures, female control and Sirt1^over mice were mated with wild-type male mice, and then the embryo implantation was examined at the morning of GD7.5. While the control mice showed normal number of implantation sites (7.75 ± 0.48), Sirt1^over mice did not form any implantation sites (n = 4/genotype) (FIG.5B panel C). These results revealed that defect of implantation is 1 of the causes of the subfertility observed in Sirt1^over mice. Next, we examined the impact of overexpression of Sirt1 on decidualization using an artificial decidualization model. Control mice displayed a decidual uterine horn that responded well to this artificial induction. However, Sirt1^over mice exhibited a significant defect (P < 0.05) in the decidual response (n = 4/genotype) (FIG.5B panel D). These results suggest that Sirt1^over mice were subfertile due to defective embryo implantation and decidualization. In normal human controls (n = 30), SIRT1 immunostaining was undetectable during the proliferative and secretory phase endometrium but dramatically elevated at menses (p < 0.001). In endometriosis cases (n = 39), SIRT1 was uniformly elevated in both proliferative and secretory phases (FIGS.6A-6B). The levels of SIRT1 was significantly higher in both the stromal and epithelial cells of endometriosis patients compared to women without endometriosis. As levels of SIRT1 protein were significantly increased in the menstrual tissues in normal women and the levels of SIRT1 were not significantly different between control menses (n = 9) and endometriosis patients during both proliferative phase and secretory phase suggest that SIRT1 is an important component of menstruation, but aberrant overexpression of SIRT1 is integral to the pathogenesis of endometriosis. Conclusions: P4-resistance is a natural phenomenon, mediated by SIRT1, and likely required for normal menstruation in women and implantation in the mouse. Over-expression of SIRT1 leads to worsening endometriosis in our mouse model and is associated with a down-regulation in P4-induced genes. In normal human controls, SIRT1 appears only at menses and may play a role in expediting the transition from secretory to proliferative state. Timing of SIRT1 expression appears vital for normal physiologic P4-resistance, with functions at menses and implantation. Infertility due to SIRT1/P4 resistance may be treatable with a SIRT1 inhibitor. Uterine-specific SIRT1 overexpression results in nonreceptive endometrium: In the rodent uterus, E2 induces the proliferation of luminal and glandular epithelial cells at GD 1.5 to 2.5. Such cell proliferation is redirected from the epithelial to the stromal cell by P stimuli after GD 3.5. Stromal cells proliferate and differentiate to specialized maternal tissue referred to as the decidua that should be necessary to maintain pregnancy. To determine whether the proliferation of endometrial cells is dysregulated in the pre- implantation period by overexpression of Sirt1, we examined the change in the spatial distribution of proliferative marker Ki-67 in the uteri of Sirt1^over mice at GD 3.5 using immunohistochemical staining (n = 5/genotype) (FIG.7 panel A). In control mice, cell proliferation is reduced in epithelial cells prior to embryo attachment and is increased in stromal cells undergoing decidualization in preparation for implantation at GD 3.5. However, cell proliferation in endometrial epithelial compartments was significantly increased at GD 3.5 in Sirt1^over mice compared to control mice (FIG.7 panels A and B). Furthermore, the expression of E2 target genes, Clca3, Muc-1, and Ltf, was significantly increased in Sirt1^over mice (n = 5/genotype) (FIG.7 panel C), but the expression of P4 target genes, Fst, Klf15, Ptch1, and Gli1, was significantly decreased in Sirt1^over mice (n = 5/ genotype) (FIG.7 panel D). These results suggest that Sirt1 overexpression results in a nonreceptive endometrium due to P4 resistance. P resistance in endometriosis may be associated with epigenetic chromatin changes that determine the intrinsic responsiveness of endometrial cells to differentiation cues. We examined whether SIRT1 physically interacts with PR-A or PR-B protein using immunoprecipitation analysis. We transfected Ishikawa cells with PGR constructs expressing either human PR-A or PR-B. The lysates were then immunoprecipitated with anti-SIRT1 antibodies, followed by Western blot analysis using anti-PGR antibody. The immunoprecipitation results showed that SIRT1 physically interacts with PR-A, not PR-B (FIG.7 panel E). Next, we performed a semiquantitative analysis of the PGR levels in the endometrium of Sirt1^over mice to determine if SIRT1 overexpression suppresses PGR expression. Our IHC and HSCORE analysis showed that the expression of PGR did not change in the uterus of Sirt1^over mice (n = 5/genotype) (FIG.7 panels F and G). These results suggest a transcriptional repressor function for SIRT1 on PGR target genes through physical interaction with PR-A but not regulation of PGR expression in the endometrium. Endometriosis Induces SIRT1 Overexpression in the Eutopic Endometrium: IHC analysis in eutopic endometrium showed that SIRT1 proteins were weakly detected in the endometrium from the proliferative phase and early, mid-, and late secretory phases in women without endometriosis. However, the expression of SIRT1 is significantly higher in eutopic endometrium from women with endometriosis compared to controls (FIGS. 6A-6B). To further determine whether SIRT1 expression is dysregulated after endo- metriosis development, we surgically induced endometriosis in female mice using autologous endometrial tissue transfer. SIRT1 protein amounts were significantly higher in the eutopic endometrium from mice with endometriosis compared to the sham group (n = 5/ model) (FIG.8 panel A). These results suggest that endometriosis results in overexpression of SIRT1 in the eutopic endometrium. Sirt1 Overexpression in Endometriotic Lesion Results in an Increase of Endometriosis Development: To assess the effect of SIRT1 overexpression in endometriosis development, we used SRT1720, a SIRT1 agonist, in our mouse endometriosis model. After endometriosis was surgically induced in Pgr^cre/+Rosa26^mTmG/+ mice, the mice were orally administrated with SRT1720 (1 mg/kg) or vehicle for 1 month. One month after the endometriosis induction, we examine the number of endometriotic lesions with green fluorescent protein expression in the mice. The number of endometriotic lesions was significantly increased in the SRT1720 group compared to the vehicle group (FIG.8 panel B). To validate the effect of SIRT1 overexpression and exclude any off-target effects of SRT1720, we examined the effect of uterine specific Sirt1 overexpression in endometriosis. Endometriosis was surgically induced in control (Pgr^cre/+ Rosa26^mTmG/+) and Pgr^cre/+Rosa26^Sirt1/mTmG (Sirt1^overRosa26^mTmG) mice by inoculating autologous endometrial tissue into the peritoneal cavity. Sirt1^overRosa26^mTmG endometrial tissue induced a significantly increased incidence of endometriotic lesions compared to controls (n = 3/genotype) (FIG.8 panel C). EX-527, a SIRT1 Inhibitor, Restores Implantation Failure in Sirt1^Over Mice and Suppresses Endometriosis Development in Mouse: EX-527 is a selective SIRT1 inhibitor (IC5038 nM) identified from a high throughput screen (Solomon et al.1994 J Endocrinol 140(2):239-249). We evaluated the effect of EX-527 on nonreceptive endometrium and implantation failure of Sirt1^over mice. Sirt1^over mice were treated with the administration of vehicle or 2.5 mg/kg/day EX-527 at GD3.5. The mice were mated with wild-type male mice and examined implantation at GD7.5. While the vehicle group showed implantation failure at GD7.5, EX-527 treatment reversed the deleterious effects of SIRT1 overexpression to restore implantation (n = 4/treatment) (FIG.9 panel A). EX-527 can cause neural tube defects, ventral edema formations, and gastrointestinal malformations in Xenopus laevis embryos (Ohata et al.2014 Dev Growth Differ.56(6):460-468). In this study, we examined the effect of EX-527 on embryo implantation in mice. Although a high dose of EX-527 (2.5 mg/kg/day) causes an implantation defect, low dose (0.5 mg/kg/day) reveals normal implantation (FIG.9 panel B). Next, endometriosis was induced in 8-week-old fertile female mice (Pgr^cre/+Rosa26^mTmG/+), and the mice were treated with vehicle or 0.5 mg/kg EX-527 for 2 weeks (n = 5/treatment) to evaluate the effect of SIRT1 on endometriosis. After EX-527 treatment, GFP endometriosis-like lesions were counted and removed under a fluorescence dissecting microscope. Intraperitoneal administration of EX-527 at a dose of 0.5 mg/kg/day for 2 weeks significantly reduced the number of endometriotic lesions compared to the control group (FIG.9 panel C). These data further corroborate the data shown and described in FIGS.1, 2, and 5A. Example 2: Estrogen is a potent proliferation-inducing steroid in the endometrium that works through an estrogen receptor (ER). ER is down-regulated by progesterone. In endometriosis, ER are not normally down-regulated by progesterone. Endometrial cell line that over- expressed SIRT1 had exaggerated proliferation and were resistance to chemotherapy. EX-527 specifically suppressed this growth, through its role in suppressing SIRT1-related progesterone resistance. Progesterone is absolutely required for uterine implantation, decidualization, and maintenance of pregnancy. Infertile women with endometriosis display epithelial defects in surface biomarkers and markedly reduced decidualization associated with impaired uterine receptivity. How endometriosis contributes to infertility remains elusive but we hypothesize this directly involves progesterone resistance through SIRT1 over-expression. A potent inducer of SIRT1, resveratrol, inhibits decidualization by down-regulating CRABPII, a known target of SIRT1, and also decreases IVF success rates when used as a supplement before transfer. Knock-down of SIRT1 restored normal decidualization. We and others are currently using endometriotic human endometrial stromal cells hESCs that have been decidualized in vitro from women and baboons to demonstrate defective decidualization in vitro. These data coupled with animal data suggest that SIRT1 is the primary driver of progesterone resistance and that this phenomenon can be reversed using EX-527 (Selisistat). Endometriosis affects millions of women. The specific problem addressed by this application relates to the phenomenon of progesterone resistance in the setting of In Vitro Fertilization (IVF) failures. There were 284,385 cycles completed in 2017 recorded by the CDC. Of those up to half of the failures may be caused by progesterone resistance due to SIRT1 over-expression. There were only 21% live births from these attempts (224,664 failures). Since IVF can fail for many reasons, we conservatively estimate that 50,000 individuals with IVF failure exhibit SIRT1 over-expression with progesterone resistance. These women may benefit from EX-527 treatments in the setting of IVF. EX-527 can optionally be administered alone and/or in combination with progesterone treatment. The foregoing is illustrative of the present invention, and is not to be construed as limiting thereof. The invention is defined by the following claims, with equivalents of the claims to be included therein.

Claims

THAT WHICH IS CLAIMED IS: 1. A method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and g) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist.

2. A method of diagnosing and treating infertility in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) diagnosing the subject as having infertility when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre- determined cut-off value, as measured in a sample of endometrium from the subject obtained; and e) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist.

3. The method of claim 2, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%. 4. The method of claim 3, wherein the pre-determined cut-off value is selected from the group consisting of 1.0, 1.1, 1.2, 1.3, 1.

4, 1.5, 1.6, 1.7, 1.8, 1.9, and 2.0.

5. A method for increasing the likelihood of implantation of an embryo in a subject with decreased endometrial receptivity due to overexpression of a SIRT1 gene, comprising administering to the subject having overexpression of a SIRT1 gene an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist.

6. A method of treating infertility in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin- releasing hormone (GnRH) agonist.

7. A method of treating endometriosis in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin- releasing hormone (GnRH) agonist.

8. A method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and e) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin- releasing hormone (GnRH) agonist.

9. A method of diagnosing and treating endometriosis in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression detected in (b); d) diagnosing the subject as having endometriosis when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre- determined cut-off value, as measured in a sample of endometrium from the subject; and e) treating the endometriosis in the subject by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin- releasing hormone (GnRH) agonist.

10. The method of claim 9, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%.

11. A method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis and/or infertility when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; d) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and g) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (f), wherein a decrease in (f) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (f) relative to (b) indicates that the treatment can be continued or increased.

12. A method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) diagnosing the subject as having endometriosis and/or infertility when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value; e) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; h) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and i) comparing the HSCORE of (c) with the HSCORE of (h), wherein a decrease in the HSCORE of (h) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (h) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased.

13. The method of claim 12, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%.

14. A method of managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; d) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (c); e) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and f) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (e), wherein a decrease in (e) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (e) relative to (b) indicates that the treatment can be continued or increased.

15. A method for managing treatment of endometriosis and/or infertility and/or endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) treating the endometriosis and/or infertility and/or endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and h) comparing the HSCORE of (c) with the HSCORE of (g), wherein a decrease in the HSCORE of (g) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (g) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased.

16. The method of claim 15, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%.

17. A method of managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) treating the endometriosis and/or infertility by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; d) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (c); e) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and f) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (e), wherein a decrease in (e) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (e) relative to (b) indicates that the treatment can be continued or increased.

18. A method for managing treatment of endometriosis and/or infertility in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) treating the endometriosis and/or infertility in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; e) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (d); f) detecting a level of expression of a SIRT1 gene product in the subsequent sample; g) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and h) comparing the HSCORE of (c) with the HSCORE of (g), wherein a decrease in the HSCORE of (g) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (g) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased.

19. The method of claim 18, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%.

20. A method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; and e) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist.

21. A method of diagnosing and treating endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product detected in (b); d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE calculated for a level of expression of a SIRT1 gene product that is greater than a pre-determined cut-off value, as measured in a sample of endometrium from the subject; and e) administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist.

22. The method of claim 21, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%.

23. A method of treating endometriosis derived ovarian cancer in a subject in need thereof, comprising administering to a subject having overexpression of a SIRT1 gene product an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K- ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist.

24. A method of managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject, optionally obtained during the first and/or second half (e.g., secretory phase and/or proliferative phase) of the subject's menstrual cycle; b) detecting a level of expression of a SIRT1 gene product in the sample; c) comparing the level of expression detected in (b) with the level of expression of a SIRT1 gene product in a sample of endometrium obtained from a control subject, optionally obtained during the first and/or the second half (e.g., secretory phase and/or proliferative phase) of the subject's menstrual cycle; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has a level of expression of the SIRT1 gene product greater than the level of expression of the SIRT1 gene product of the control subject; e) treating the endometriosis derived ovarian cancer by administering to the subject an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; and h) comparing the level of expression of the SIRT1 gene product detected in (b) with the level of expression of the SIRT1 gene product detected in (g), wherein a decrease in (g) relative to (b) in a subject indicates that the treatment can be halted or reduced, and an increase or no change in (g) relative to (b) indicates that the treatment can be continued or increased.

25. A method for managing treatment of endometriosis derived ovarian cancer in a subject, comprising: a) obtaining a first sample of endometrium from the subject; b) detecting a level of expression of a SIRT1 gene product in the first sample; c) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the first sample; d) diagnosing the subject as having endometriosis derived ovarian cancer when the subject has an HSCORE based on the level of expression of the SIRT1 gene product that is greater than a pre-determined cut-off value; e) treating the endometriosis derived ovarian cancer in the subject by administering an effective amount of EX-527, optionally in combination with an effective amount of progesterone, a treatment that enhances progesterone activity, an effective amount of a K-ras inhibitor, a treatment that blocks or reduces K-ras activity, an effective amount of a BCL6 inhibitor, a treatment that blocks or reduces BCL6 activity, by surgical removal of some or all of the endometriosis, and/or administration to the subject of an effective amount of a gonadotropin-releasing hormone (GnRH) agonist; f) obtaining a subsequent sample of endometrium from the subject at one or more time points following step (e); g) detecting a level of expression of a SIRT1 gene product in the subsequent sample; h) calculating an HSCORE for the subject based on the level of expression of the SIRT1 gene product in the subsequent sample; and i) comparing the HSCORE of (c) with the HSCORE of (h), wherein a decrease in the HSCORE of (h) indicates that the treatment of the endometriosis and/or infertility can be halted or reduced, and no change or an increase in the HSCORE of (h) to a value greater than or equal to a pre-determined cut-off value indicates that treatment of the endometriosis and/or infertility can be continued or increased.

26. The method of claim 25, wherein the HSCORE is calculated using the following equation: HSCORE =∑ Pi (i + 1)/100, where i = the intensity of staining of cells in the sample with a value of 1 being low staining, 2 being moderate staining, and 3 being strong staining, and Pi being the percentage of stained cells in the sample for each intensity, varying from 0-100%.