Mediator kinase inhibition further activates super-enhancer-associated genes in AML
Henry E. Pelish,
Brian B. Liau,
Ioana I. Nitulescu,
Anupong Tangpeerachaikul,
Zachary C. Poss,
Diogo H. Da Silva,
Brittany T. Caruso,
Alexander Arefolov,
Olugbeminiyi Fadeyi,
Amanda L. Christie,
Karrie Du,
Deepti Banka,
Elisabeth V. Schneider,
Anja Jestel,
Ge Zou,
Chong Si,
Christopher C. Ebmeier,
Roderick T. Bronson,
Andrei V. Krivtsov,
Andrew G. Myers,
Nancy E. Kohl,
Andrew L. Kung,
Scott A. Armstrong,
Madeleine E. Lemieux,
Dylan J. Taatjes and
Matthew D. Shair ()
Additional contact information
Henry E. Pelish: Harvard University
Brian B. Liau: Harvard University
Ioana I. Nitulescu: Harvard University
Anupong Tangpeerachaikul: Harvard University
Zachary C. Poss: University of Colorado
Diogo H. Da Silva: Harvard University
Brittany T. Caruso: Harvard University
Alexander Arefolov: Harvard University
Olugbeminiyi Fadeyi: Harvard University
Amanda L. Christie: Lurie Family Imaging Center, Dana-Farber Cancer Institute
Karrie Du: Harvard University
Deepti Banka: Children's Hospital
Elisabeth V. Schneider: Proteros Biostructures GmbH
Anja Jestel: Proteros Biostructures GmbH
Ge Zou: Harvard University
Chong Si: Harvard University
Christopher C. Ebmeier: University of Colorado
Roderick T. Bronson: Dana-Farber Cancer Institute
Andrei V. Krivtsov: Memorial Sloan Kettering Cancer Center
Andrew G. Myers: Harvard University
Nancy E. Kohl: Lurie Family Imaging Center, Dana-Farber Cancer Institute
Andrew L. Kung: Columbia University Medical Center
Scott A. Armstrong: Memorial Sloan Kettering Cancer Center
Madeleine E. Lemieux: Bioinfo
Dylan J. Taatjes: University of Colorado
Matthew D. Shair: Harvard University
Nature, 2015, vol. 526, issue 7572, 273-276
Abstract:
A small-molecule inhibitor of the Mediator-associated kinases CDK8 and CDK19 inhibits growth of acute myeloid leukaemia (AML) cells and induces upregulation of super-enhancer-associated genes with tumour suppressor and lineage-controlling functions; Mediator kinase inhibition therefore represents a promising therapeutic approach for AML.
Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:526:y:2015:i:7572:d:10.1038_nature14904
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DOI: 10.1038/nature14904
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