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METHOD FOR USING A HISTONDEACETYLASE INHIBITOR AND MONITORING BIOMARKERS IN COMBINED THERAPY
专利权人:
Инк. (US);Фармасайкликс
发明人:
ЭДИМУЛАМ Шанти (US),БАГГИ Джозеф Дж. (US),МАГДА Даррен (US),МИЛЛЕР Ричард (US)
申请号:
RU2011148293/15
公开号:
RU2011148293A
申请日:
2011.11.29
申请国别(地区):
RU
年份:
2013
代理人:
摘要:
1. A method of treating a disease, disorder or condition caused by a defect in a non-homologous reunion of DNA ends, wherein: (a) a therapeutically effective amount of at least one agent is administered to a patient suffering from a disease, disorder or condition caused by a defect in a non-homologous reunification of DNA ends which inhibits the activity of RAD51, interrupts the formation of RAD51 foci, or interrupts the assembly of a functional repair complex for homologous DNA recombination; and (b) the patient is treated for damage to the cellular DNA. 2. The method according to claim 1, wherein at least one agent that inhibits RAD51 activity interrupts the formation of RAD51 foci or interrupts the assembly of a functional repair complex for homologous DNA recombination, is a therapeutically effective histone deacetylase inhibitor or a pharmaceutically acceptable derivative thereof. The method of claim 1, wherein the defect in the non-homologous reunion of the DNA ends comprises a defect in a gene selected from the group consisting of: Ku70, Ku80, Ku86, Ku, PRKDC, LIG4, XRCC4, DCLREIC and XLF.4. The method of claim 1, wherein the disease, disorder or condition is a cancer selected from breast cancer, colon cancer, colon and colon carcinomas, non-small cell lung cancer, small cell lung cancer, liver cancer, ovarian cancer, prostate cancer, cancer cervical cancer, bladder cancer, gastric carcinomas, gastrointestinal stromal tumors, pancreatic cancer, germ cell tumors, mast cell tumors, neuroblastoma, mastocytosis, testicular cancer, glioblastoma, astrocy about1. Способ лечения заболевания, расстройства или состояния, обусловленного дефектом в негомологичном воссоединении концов ДНК, при котором:(а) пациенту, страдающему заболеванием, расстройством или состоянием, обусловленным дефектом в негомологичном воссоединении концов ДНК, вводят терапевтически эффективное количество по меньшей мере одного агента, который ингибирует активность RAD51, прерывает образование фоку
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