BET inhibition decreases HMGCS2 and sensitizes resistant pancreatic tumors to gemcitabine.

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第一作者： Aubrey L,Miller

第一单位： Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA.

作者： Aubrey L,Miller ^[1] ; Samuel C,Fehling ^[1] ; Rebecca B,Vance ^[1] ; Dongquan,Chen ^[2] ; Eric Josh,Brown ^[1] ; M Iqbal,Hossain ^[1] ; Eric O,Heard ^[1] ; Shaida A,Andrabi ^[3] ; Hengbin,Wang ^[4] ; Eddy S,Yang ^[5] ; Donald J,Buchsbaum ^[6] ; Robert C A M,van Waardenburg ^[1] ; Susan L,Bellis ^[7] ; Karina J,Yoon ^[8]

作者单位： Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA. ^[1] Department of Preventive Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. ^[2] Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, USA. ^[3] Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL, USA. ^[4] Department of Radiation Oncology, University of Alabama at Birmingham, Birmingham, AL, USA. ^[5] Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL, USA. ^[6] Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, USA. ^[7] Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: kyoon@uab.edu. ^[8]

关键词 BET bromodomain inhibitor (BETi)Gemcitabine resistance (gemR)HMG-CoA synthase 2 (HMGCS2)Pancreatic cancer Patient-derived xenograft (PDX) models