mTOR inhibitors suppress homologous recombination repair and synergize with PARP inhibitors via regulating SUV39H1 in BRCA-proficient triple-negative breast cancer

Clinical Cancer Research

Volumn 22, Issue 7, 2016, Pages 1699-1712

  Mo, Wei ^a   Liu, Qingxin ^a   Lin, Curtis Chun Jen ^a   Dai, Hui ^a   Peng, Yang ^a   Liang, Yulong ^b   Peng, Guang ^a   Meric Bernstam, Funda ^a   Mills, Gordon B ^a   Li, Kaiyi ^b   Lin, Shiaw Yih ^a  

^a UNIVERSITY OF TEXAS   (United States)

^b BAYLOR COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

5 [2 (2,6 DIMETHYLMORPHOLINO) 4 MORPHOLINOPYRIDO[2,3 D]PYRIMIDIN 7 YL] 2 METHOXYBENZENEMETHANOL; BRCA PROTEIN; EVEROLIMUS; MAMMALIAN TARGET OF RAPAMYCIN INHIBITOR; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE INHIBITOR; OLAPARIB; ONCOPROTEIN; SUV39H PROTEIN; TALAZOPARIB; UNCLASSIFIED DRUG; BRCA1 PROTEIN; BRCA2 PROTEIN; METHYLTRANSFERASE; PROTEIN KINASE INHIBITOR; REPRESSOR PROTEIN; SUV39H1 PROTEIN, HUMAN; TARGET OF RAPAMYCIN KINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CANCER CELL LINE; CONTROLLED STUDY; DOUBLE STRANDED DNA BREAK; DRUG EFFECT; DRUG MECHANISM; DRUG POTENTIATION; FEMALE; HUMAN; HUMAN CELL; IN VITRO STUDY; IN VIVO STUDY; MICROARRAY ANALYSIS; MOUSE; NONHUMAN; PRIORITY JOURNAL; RECOMBINATION REPAIR; TRIPLE NEGATIVE BREAST CANCER; TUMOR XENOGRAFT; ANIMAL; ANTAGONISTS AND INHIBITORS; DISEASE MODEL; DRUG EFFECTS; DRUG SCREENING; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; PATHOLOGY; TRIPLE NEGATIVE BREAST NEOPLASMS; TUMOR CELL LINE;

ANIMALS; BRCA1 PROTEIN; BRCA2 PROTEIN; CELL LINE, TUMOR; DISEASE MODELS, ANIMAL; DRUG SYNERGISM; FEMALE; GENE EXPRESSION REGULATION, NEOPLASTIC; HUMANS; METHYLTRANSFERASES; MICE; POLY(ADP-RIBOSE) POLYMERASE INHIBITORS; PROTEIN KINASE INHIBITORS; RECOMBINATIONAL DNA REPAIR; REPRESSOR PROTEINS; TOR SERINE-THREONINE KINASES; TRIPLE NEGATIVE BREAST NEOPLASMS; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 84964331077     PISSN: 10780432     EISSN: 15573265     Source Type: Journal    
DOI: 10.1158/1078-0432.CCR-15-1772     Document Type: Article

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