US20090062196A1 - Compositions and methods of treating cancer - Google Patents

Compositions and methods of treating cancer Download PDF

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US20090062196A1
US20090062196A1 US11/975,997 US97599707A US2009062196A1 US 20090062196 A1 US20090062196 A1 US 20090062196A1 US 97599707 A US97599707 A US 97599707A US 2009062196 A1 US2009062196 A1 US 2009062196A1
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dna
pathway
cell
cells
repair
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US11/975,997
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Alan D'Andrea
David T. Weaver
Markus Grompe
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DNA REPAIR Co
Dana Farber Cancer Institute Inc
Oregon Health and Science University
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Individual
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Assigned to THE DNA REPAIR COMPANY reassignment THE DNA REPAIR COMPANY ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: WEAVER, DAVID T.
Assigned to DANA FARBER CANCER INSTITUTE, INC. reassignment DANA FARBER CANCER INSTITUTE, INC. ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: D'ANDREA, ALAN
Assigned to OREGON HEALTH SCIENCES UNIVERSITY reassignment OREGON HEALTH SCIENCES UNIVERSITY ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: GROMPE, MARKUS
Assigned to DANA FARBER CANCER INSTITUTE, INC. reassignment DANA FARBER CANCER INSTITUTE, INC. ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: KENNEDY, RICHARD
Assigned to NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT reassignment NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT CONFIRMATORY LICENSE (SEE DOCUMENT FOR DETAILS). Assignors: DANA-FARBER CANCER INST
Priority to US14/948,914 priority patent/US10738310B2/en
Assigned to NATIONAL INSTITUTES OF HEALTH-DIRECTOR DEITR reassignment NATIONAL INSTITUTES OF HEALTH-DIRECTOR DEITR CONFIRMATORY LICENSE (SEE DOCUMENT FOR DETAILS). Assignors: DANA-FARBER CANCER INSTITUTE
Priority to US16/537,899 priority patent/US20200140868A1/en
Abandoned legal-status Critical Current

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    • C12Q1/6876—Nucleic acid products used in the analysis of nucleic acids, e.g. primers or probes
    • C12Q1/6883—Nucleic acid products used in the analysis of nucleic acids, e.g. primers or probes for diseases caused by alterations of genetic material
    • C12Q1/6886—Nucleic acid products used in the analysis of nucleic acids, e.g. primers or probes for diseases caused by alterations of genetic material for cancer
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    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
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    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P35/00—Antineoplastic agents
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    • A—HUMAN NECESSITIES
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    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
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    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
    • G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
    • G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
    • G01N33/53—Immunoassay; Biospecific binding assay; Materials therefor
    • G01N33/575—Immunoassay; Biospecific binding assay; Materials therefor for cancer
    • G01N33/5758—Immunoassay; Biospecific binding assay; Materials therefor for cancer involving compounds serving as markers for tumours, cancers or neoplasias, e.g. cellular determinants, receptors, heat shock/stress proteins, A-protein, oligosaccharides or metabolites
    • G01N33/57595—Immunoassay; Biospecific binding assay; Materials therefor for cancer involving compounds serving as markers for tumours, cancers or neoplasias, e.g. cellular determinants, receptors, heat shock/stress proteins, A-protein, oligosaccharides or metabolites involving intracellular compounds
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    • G01N2333/46—Assays involving biological materials from specific organisms or of a specific nature from animals; from humans from vertebrates
    • G01N2333/47—Assays involving proteins of known structure or function as defined in the subgroups
    • G01N2333/4701—Details
    • G01N2333/4716—Complement proteins, e.g. anaphylatoxin, C3a, C5a

Definitions

  • a method of increasing the responsiveness of a cancer cell to a DNA crosslinking agent or ionizing radiation includes contacting the cancer cell with an inhibitor of the homologous recombination and crosslinking repair (FA/HR) DNA repair pathway.
  • the method of identifying the responsiveness of a cancer cell to a MAP2KAP2 inhibitor includes detecting phosphorylation of MAP2KAP2, where the presence of the phosphorylation indicates the cell is sensitive to a MAP2KAP2 inhibitor, whereas an absence of the phosphorylation indicates the cell is resistant to a MAP2KAP2 inhibitor.
  • the reactivities of a binding member such as an antibody on normal and test samples may be determined by any appropriate means. Tagging with individual reporter molecules is one possibility.
  • the reporter molecules may directly or indirectly generate detectable, and preferably measurable, signals.
  • the linkage of reporter molecules may be directly or indirectly, covalently, e.g. via a peptide bond or non-covalently. Linkage via a peptide bond may be as a result of recombinant expression of a gene fusion encoding binding molecule (e.g. antibody) and reporter molecule.
  • FIG. 3 Panel F, shows a Western blot assessing ATM auto-phosphorylation and FANCD2 monoubiqitination in FA pathway deficient EUFA326 cells (lanes 1 and 3) and FA pathway corrected EUFA326G cells (lanes 2 and 4) at baseline (lanes 1 and 2) and 6 hrs after 10 Gy ionizing radiation (lanes 3 and 4).
  • FIG. 3 Panel G. shows a Comet assay comparing DNA breaks in EUFA326 versus EUFA326G cells 72 hrs after transfection with siRNA to ATM.
  • Panel (i) shows a graphical description of DNA damage as measured by Comet assay. The Y axis represents mean comet tail length, a measure of DNA breaks.
  • FIG. 19C The ability of the FANCE mutant proteins to restore FANCD2 monoubiquitination was examined ( FIG. 19C ). As previously described FLAG-FANCEwt restored FANCD2 monoubiquitination ( FIG. 19C , lanes 6-10), and DNA damage generated by IR further activated FANCD2 monoubiquitination.
  • the double mutant FANCE (FLAG-TS/AA) also restored monoubiquitination of FANCD2.
  • Cells expressing the double mutant FANCE (FLAG-TS/AA) had elevated basal levels of FANCD2 monoubiquitination ( FIG. 19C , compare lanes 11 and 6), and failed to exhibit further FANCD2 monoubiquitination following DNA damage ( FIG. 19C , lanes 11-15).
  • EUFA130 and EUFA130+E cells were plated at low density, and subsequently treated with 1 uM of the Chk1 inhibitor G06976 and then tested for the distribution of cells at different cell cycle phases. It was found that the Chk1 inhibitor caused an increased fraction of cells in G1 and the subG1 cell population by propidium iodide staining. SubG1 cells are indicative of cells entering apoptosis.

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US11/975,997 2006-10-20 2007-10-22 Compositions and methods of treating cancer Abandoned US20090062196A1 (en)

Priority Applications (3)

Application Number Priority Date Filing Date Title
US11/975,997 US20090062196A1 (en) 2006-10-20 2007-10-22 Compositions and methods of treating cancer
US14/948,914 US10738310B2 (en) 2006-10-20 2015-11-23 Treating cancer deficient in FANCA, FANCD2, FANCE, or FANCG with an ATM inhibitor
US16/537,899 US20200140868A1 (en) 2006-10-20 2019-08-12 Compositions and methods for treating cancer

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US85320806P 2006-10-20 2006-10-20
US89560607P 2007-03-19 2007-03-19
US11/975,997 US20090062196A1 (en) 2006-10-20 2007-10-22 Compositions and methods of treating cancer

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US14/948,914 Continuation US10738310B2 (en) 2006-10-20 2015-11-23 Treating cancer deficient in FANCA, FANCD2, FANCE, or FANCG with an ATM inhibitor

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US11/975,997 Abandoned US20090062196A1 (en) 2006-10-20 2007-10-22 Compositions and methods of treating cancer
US14/948,914 Active 2027-12-16 US10738310B2 (en) 2006-10-20 2015-11-23 Treating cancer deficient in FANCA, FANCD2, FANCE, or FANCG with an ATM inhibitor
US16/537,899 Abandoned US20200140868A1 (en) 2006-10-20 2019-08-12 Compositions and methods for treating cancer

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US16/537,899 Abandoned US20200140868A1 (en) 2006-10-20 2019-08-12 Compositions and methods for treating cancer

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EP (1) EP2092083A2 (https=)
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US10676791B2 (en) 2014-07-25 2020-06-09 Inserm(Institut National De La Sante Et De La Recherche Medicale) Methods for predicting response to DNA repair pathway inhibitors in diffuse large B-cell lymphoma
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CN120741580A (zh) * 2025-06-27 2025-10-03 江苏香地化学有限公司 一种用于检测丝裂霉素c的分子印迹比率型工作电极及其制备方法和应用

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