The combination of BET and PARP inhibitors is synergistic in models of cholangiocarcinoma

Our previous finding that the BET inhibitor (BETi) JQ1 increases levels of the DNA damage marker γH2AX suggested that JQ1 might enhance the sensitivity of tumor cells to PARP inhibitors (PARPi), which are selectively toxic to cells that harbor relatively high levels of DNA damage. To address this hy...

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Veröffentlicht in:	Cancer letters 2020-01, Vol.468, p.48-58
Hauptverfasser:	Fehling, Samuel C., Miller, Aubrey L., Garcia, Patrick L., Vance, Rebecca B., Yoon, Karina J.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Combined Chemotherapy Protocols - pharmacology Antineoplastic Combined Chemotherapy Protocols - therapeutic use Apoptosis Azepines - pharmacology Azepines - therapeutic use BET inhibitors Bile Duct Neoplasms - drug therapy Bile Duct Neoplasms - genetics Bile Duct Neoplasms - pathology c-Myc Cancer Cell cycle Cell Cycle Proteins - antagonists & inhibitors Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell Line, Tumor Cholangiocarcinoma Cholangiocarcinoma - drug therapy Cholangiocarcinoma - genetics Cholangiocarcinoma - pathology Combination indices Cytotoxicity Deoxyribonucleic acid DNA DNA damage Drug Synergism Experiments Female Gene Expression Regulation, Neoplastic - drug effects Humans Inhibitors Mice PARP inhibitors Phthalazines - pharmacology Phthalazines - therapeutic use Piperazines - pharmacology Piperazines - therapeutic use Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerase Inhibitors - pharmacology Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use Proteins RNA, Small Interfering - metabolism RNAi Targeted cancer therapy Transcription Factors - antagonists & inhibitors Transcription Factors - genetics Transcription Factors - metabolism Triazoles - pharmacology Triazoles - therapeutic use Tumor cells Tumors Xenograft Model Antitumor Assays Xenografts
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