JPWO2020242330A5 - - Google Patents

Download PDF

Info

Publication number
JPWO2020242330A5
JPWO2020242330A5 JP2022516587A JP2022516587A JPWO2020242330A5 JP WO2020242330 A5 JPWO2020242330 A5 JP WO2020242330A5 JP 2022516587 A JP2022516587 A JP 2022516587A JP 2022516587 A JP2022516587 A JP 2022516587A JP WO2020242330 A5 JPWO2020242330 A5 JP WO2020242330A5
Authority
JP
Japan
Prior art keywords
fancm
composition
alt
activity
expression
Prior art date
Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Pending
Application number
JP2022516587A
Other languages
Japanese (ja)
Other versions
JP2022534138A (en
Publication date
Priority claimed from GBGB1907518.3A external-priority patent/GB201907518D0/en
Application filed filed Critical
Priority claimed from PCT/PT2020/050021 external-priority patent/WO2020242330A2/en
Publication of JP2022534138A publication Critical patent/JP2022534138A/en
Publication of JPWO2020242330A5 publication Critical patent/JPWO2020242330A5/ja
Pending legal-status Critical Current

Links

Claims (21)

テロメア代替伸長(ALT)細胞の生存能及び/又はALT細胞の成長を阻害する方法における使用のための組成物であって、前記方法が、前記ALT細胞におけるファンコーニ貧血相補群M(FANCM)の発現又は活性を低減させる工程を含む、組成物。 1. A composition for use in a method of inhibiting telomere replacement elongation (ALT) cell viability and/or ALT cell growth , said method comprising: A composition comprising reducing expression or activity. FANCMの発現又は活性が、FANCMアンタゴニストを個体に投与することによって低減される、請求項1に記載の組成物。 2. The composition of claim 1, wherein FANCM expression or activity is reduced by administering a FANCM antagonist to the individual. 前記FANCMアンタゴニストが、サプレッサー核酸である、請求項2に記載の組成物。 3. The composition of claim 2 , wherein said FANCM antagonist is a suppressor nucleic acid. BLM及び/又はBRCA1の活性又は発現が、前記ALT細胞において低減されない、請求項1に記載の組成物。 2. The composition of claim 1 , wherein BLM and/or BRCA1 activity or expression is not reduced in said ALT cells. 前記ALT細胞が、間葉系又は上皮がん細胞である、請求項1に記載の組成物。 2. The composition of claim 1 , wherein said ALT cells are mesenchymal or epithelial cancer cells. 前記方法が、FANCM-RMI相互作用を崩壊させる工程、及び/又はFANCMのATPアーゼ活性を阻害する工程を含む、請求項1に記載の組成物。 2. The composition of claim 1, wherein said method comprises disrupting the FANCM-RMI interaction and/or inhibiting the ATPase activity of FANCM. 阻害剤が、遺伝学的阻害剤、小分子、ペプチド及びタンパク質のいずれか1つ又は複数である、請求項6に記載の組成物。 7. The composition of claim 6 , wherein the inhibitor is any one or more of genetic inhibitors, small molecules, peptides and proteins. それを必要とする個体におけるテロメア代替伸長(ALT)がんを処置する方法における使用のための組成物であって、前記方法が、前記個体においてファンコーニ貧血相補群M(FANCM)の発現又は活性を低減させる工程を含む、組成物。 A composition for use in a method of treating telomere alternative lengthening (ALT) cancer in an individual in need thereof, said method comprising: expression or activity of Fanconi anemia complementation group M (FANCM) in said individual A composition comprising the step of reducing FANCMの発現又は活性が、FANCMアンタゴニストを前記個体に投与することによって低減される、請求項8に記載の組成物。 9. The composition of claim 8 , wherein FANCM expression or activity is reduced by administering a FANCM antagonist to said individual. 前記FANCMアンタゴニストが、FANCMの発現を低減させる、請求項9に記載の組成物。 10. The composition of claim 9 , wherein said FANCM antagonist reduces expression of FANCM. 前記FANCMアンタゴニストが、サプレッサー核酸である、請求項10に記載の組成物。 11. The composition of claim 10 , wherein said FANCM antagonist is a suppressor nucleic acid. BLM及び/又はBRCA1の活性又は発現が、ALT細胞において低減されない、請求項8から11のいずれか一項に記載の組成物。 12. The composition of any one of claims 8-11 , wherein BLM and/or BRCA1 activity or expression is not reduced in ALT cells. 前記ALTがんが、間葉系又は上皮がんである、請求項8から12のいずれか一項に記載の組成物。 13. The composition of any one of claims 8-12 , wherein the ALT cancer is a mesenchymal or epithelial cancer. 前記方法が、FANCM-RMI相互作用を崩壊させる工程、及び/又はFANCMのATPアーゼ活性を阻害する工程を含む、請求項8に記載の組成物。 9. A composition according to claim 8 , wherein the method comprises disrupting the FANCM-RMI interaction and/or inhibiting the ATPase activity of FANCM. FANCM-RMI相互作用を崩壊させる工程が、FANCM-RMI相互作用の阻害剤及び/若しくはFANCMのATPアーゼ活性の阻害剤を投与する工程、並びに/又はFANCMのATPアーゼ活性を阻害する薬剤を投与する工程を含む、請求項14に記載の組成物。 Disrupting the FANCM-RMI interaction comprises administering an inhibitor of the FANCM-RMI interaction and/or an inhibitor of the ATPase activity of FANCM and/or administering an agent that inhibits the ATPase activity of FANCM. 15. The composition of claim 14 , comprising the steps of: 阻害剤が、遺伝学的阻害剤、小分子、ペプチド及びタンパク質のいずれか1つ又は複数である、請求項14又は15に記載の組成物。 16. The composition of claim 14 or 15 , wherein the inhibitor is any one or more of genetic inhibitors, small molecules, peptides and proteins. 前記方法が、化学療法剤の同時の、逐次的な、若しくは別々の投与を更に含む、又は、前記方法が、化学療法剤の同時の、逐次的な、若しくは別々の投与を含まない、請求項15に記載の組成物。 wherein said method further comprises simultaneous, sequential or separate administration of chemotherapeutic agents, or said method does not comprise simultaneous, sequential or separate administration of chemotherapeutic agents. Item 16. The composition of Item 15 . がんに罹っている対象が、FANCM-RMI相互作用の阻害剤での処置に好適であるかどうかを同定する方法であって、前記がんがALTがんであるかどうかを決定する工程を含み、前記対象がALTがんに罹っている場合、前記対象が、FANCM-RMI相互作用の前記阻害剤での処置に好適であると同定される、方法。 A method of identifying whether a subject with cancer is suitable for treatment with an inhibitor of the FANCM-RMI interaction, said method comprising determining whether said cancer is an ALT cancer. , wherein said subject is identified as suitable for treatment with said inhibitor of FANCM-RMI interaction if said subject has ALT cancer. 対象が、FANCM-RMI相互作用の阻害剤での処置に応答しているかどうかを決定する方法であって、
対象から採取した細胞における1つ若しくは複数のテロメアにおけるゲノム不安定性の存在及び/若しくは程度を決定する工程;並びに/又は
対象から採取した細胞におけるALT活性の存在及び/若しくはレベルを決定する工程
を含む、方法。 A method of determining whether a subject is responding to treatment with an inhibitor of the FANCM-RMI interaction, comprising:
determining the presence and/or extent of genomic instability at one or more telomeres in cells taken from the subject; and/or determining the presence and/or level of ALT activity in cells taken from the subject. ,Method. 前記阻害剤が、遺伝学的阻害剤、小分子、ペプチド及びタンパク質のいずれか1つ又は複数である、請求項18又は19に記載の方法。 20. The method of claim 18 or 19 , wherein said inhibitor is any one or more of genetic inhibitors, small molecules, peptides and proteins. ALTがん細胞の死を誘発する化合物をスクリーニングする方法であって、FANCMの発現又は活性に対する試験化合物の作用を決定する工程を含み、
FANCMの発現又は活性における低減は、前記化合物が、ALT細胞において細胞死を誘発することを示す、方法。 A method of screening for a compound that induces ALT cancer cell death, comprising the steps of determining the effect of a test compound on the expression or activity of FANCM,
A method, wherein a reduction in FANCM expression or activity indicates that said compound induces cell death in ALT cells.
JP2022516587A 2019-05-24 2020-05-23 ALT cancer treatment Pending JP2022534138A (en)

Applications Claiming Priority (5)

Application Number Priority Date Filing Date Title
AU2019901766A AU2019901766A0 (en) 2019-05-24 Methods of treating ALT cancer
AU2019901766 2019-05-24
GB1907518.3 2019-05-28
GBGB1907518.3A GB201907518D0 (en) 2019-05-28 2019-05-28 Treatment of ALT cancer
PCT/PT2020/050021 WO2020242330A2 (en) 2019-05-24 2020-05-23 Treatment of alt cancers

Publications (2)

Publication Number Publication Date
JP2022534138A JP2022534138A (en) 2022-07-27
JPWO2020242330A5 true JPWO2020242330A5 (en) 2023-06-01

Family

ID=72039648

Family Applications (1)

Application Number Title Priority Date Filing Date
JP2022516587A Pending JP2022534138A (en) 2019-05-24 2020-05-23 ALT cancer treatment

Country Status (8)

Country Link
US (1) US20230149507A1 (en)
EP (1) EP3976778A2 (en)
JP (1) JP2022534138A (en)
KR (1) KR20220012339A (en)
CN (1) CN114127269A (en)
AU (1) AU2020283323A1 (en)
CA (1) CA3141464A1 (en)
WO (1) WO2020242330A2 (en)

Families Citing this family (2)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
CN113637753A (en) * 2021-08-13 2021-11-12 上海市同济医院 Bladder cancer marker lncRNA TERC based on urine exosome and application thereof
WO2024068467A1 (en) 2022-09-26 2024-04-04 Cosconati Sandro Tetrahydroquinoline compounds as antitumor agents

Family Cites Families (3)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
GB9015198D0 (en) 1990-07-10 1990-08-29 Brien Caroline J O Binding substance
CN102639713B (en) 2009-09-22 2015-09-02 儿童医学研究所 For detecting method and the assay method of substituting lengthening of telomeres (ALT) activity in cell
JP2019505562A (en) 2016-02-22 2019-02-28 ニューヨーク インスティチュート オブ テクノロジーＮｅｗ Ｙｏｒｋ Ｉｎｓｔｉｔｕｔｅ Ｏｆ Ｔｅｃｈｎｏｌｏｇｙ Methods of treating cancer by disabling BRCA1 / FANCM interaction

Similar Documents

Publication Publication Date Title
Borg et al. Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin
Terzi et al. The cell fate: senescence or quiescence
Kubli et al. AhR controls redox homeostasis and shapes the tumor microenvironment in BRCA1-associated breast cancer
Frelin et al. GATA-3 regulates the self-renewal of long-term hematopoietic stem cells
Jesus et al. Alamandine acts via MrgD to induce AMPK/NO activation against ANG II hypertrophy in cardiomyocytes
Rhee et al. Endothelial deletion of Ino80 disrupts coronary angiogenesis and causes congenital heart disease
Mantel et al. Enhancing hematopoietic stem cell transplantation efficacy by mitigating oxygen shock
Homem et al. Drosophila neuroblasts: a model for stem cell biology
La et al. Mechanisms regulating mammalian spermatogenesis and fertility recovery following germ cell depletion
Song et al. Regulation of cell growth by Notch signaling and its differential requirement in normal vs. tumor-forming stem cells in Drosophila
Ouko et al. Wnt11 signaling promotes proliferation, transformation, and migration of IEC6 intestinal epithelial cells
Sousa et al. Exit from naive pluripotency induces a transient X chromosome inactivation-like state in males
Koe et al. The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages
Kakarala et al. Cancer stem cells: implications for cancer treatment and prevention
Zhang et al. Mediator subunit MED31 is required for radial patterning of Arabidopsis roots
Qiu et al. Glucose signaling is important for nutrient adaptation during differentiation of pleomorphic African trypanosomes
Theunissen et al. Compound-specific effects of diverse neurodevelopmental toxicants on global gene expression in the neural embryonic stem cell test (ESTn)
Haftbaradaran Esfahani et al. Cell shape determines gene expression: cardiomyocyte morphotypic transcriptomes
Tao et al. A long-lived luminal subpopulation enriched with alveolar progenitors serves as cellular origin of heterogeneous mammary tumors
Jobava et al. Adaptive translational pausing is a hallmark of the cellular response to severe environmental stress
Takano et al. S100A8/MYD88/NF-қB: a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone
Slater et al. Stress-induced enzyme activation primes murine embryonic stem cells to differentiate toward the first extraembryonic lineage
Brandão et al. A regeneration-triggered metabolic adaptation is necessary for cell identity transitions and cell cycle re-entry to support blastema formation and bone regeneration
Ohm et al. Early landmark analysis of imatinib treatment in CML chronic phase: Less than 10% BCR‐ABL by FISH at 3 months associated with improved long‐term clinical outcome
La et al. Distinctive molecular features of regenerative stem cells in the damaged male germline