James E. Bradner, MD
Office phone: 617-632-6629
Website: The Bradner Laboratory
Preferred contact method: email
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Multiple myeloma, Stem cell transplantation
Area of Research
Chemical Biology and Cancer Biology
Dana-Farber Cancer Institute
450 Brookline Avenue
Dana Building D510D
Boston, MA 02215
Dr. Bradner received his MD from The University of Chicago in 1999. He completed his postgraduate training in Internal Medicine at Brigham and Women's Hospital, followed by a fellowship in Medical Oncology and Hematology at Dana-Farber Cancer Institute and Brigham and Women's Hospital. In 2005, he joined Dana-Farber and is currently a member of the Hematologic Malignancies staff.
Medical Oncology, 2005
Brigham & Women's Hospital, Medicine, 1999-2002
Dana-Farber Cancer Institute, Hematology-Oncology, 2002-2005
University of Chicago-Pritzker School of Medicine, Chicago, IL, 1999
- Damon Runyon-Rachleff Innovation Award, 2010
- Smith Family Award for Excellence in Biomedical Research, 2010
- Rising Star Award, Dunkin Donuts, 2007
- Fellow Scholar Award, American Society of Hematology, 2006
- Distinguished Excellence in Teaching Award, Brigham & Women's Hospital, 2005
- Golden Hammer Teaching Award, Harvard Medical School, 2002
- Bok Teaching Award, 1995
ResearchChemical Biology and Cancer Biology
The focus of the Bradner laboratory concerns the discovery, optimization and characterization of small-molecule modulators of gene regulatory pathways. Simply stated, we strive to develop prototype drugs which act to turn off growth genes in cancer cells by inhibiting master regulators of cell division and cellular memory. The clinical objective of our group is to deliver new therapeutics for human clinical investigation in hematologic diseases.
- Direct inhibition of the NOTCH transcription factor complex. Moellering RE, Cornejo M, Davis TN, Del Bianco C, Aster JC, Blacklow SC, Kung AL, Gilliland DG, Verdine GL, Bradner JE. Nature. 2009 Nov 12;462(7270):182-8.
- Synthesis and conformation-activity relationships of the peptide isosteres of FK228 and largazole. Bowers AA, Greshock TJ, West N, Estiu G, Schreiber SL, Wiest O, Williams RM, Bradner JE. J Am Chem Soc. 2009 Mar 4;131(8):2900-5.
- Selective inhibition of BET bromodomains. Filippakopoulos P, Qi J, Picaud S, Shen Y, Smith WB, Fedorov O, Morse EM, Keates T, Hickman TT, Felletar I, Philpott M, Munro S, McKeown MR, Wang Y, Christie AL, West N, Cameron MJ, Schwartz B, Heightman TD, La Thangue N, French CA, Wiest O, Kung AL, Knapp S, Bradner JE. Nature. 2010 Sep 24. [Epub ahead of print]
- Chemical genetic strategy identifies histone deacetylase 1 (HDAC1) and HDAC2 as therapeutic targets in sickle cell disease. Bradner JE, Mak R, Tanguturi SK, Mazitschek R, Haggarty SJ, Ross K, Chang CY, Bosco J, West N, Morse E, Lin K, Shen JP, Kwiatkowski NP, Gheldof N, Dekker J, DeAngelo DJ, Carr SA, Schreiber SL, Golub TR, Ebert BL. Proc Natl acad Sci USA. 2010 Jul 13;107(28):12617-22. Epub 2010 Jun 28.
- Chemical phylogenetics of histone deacetylases. Bradner JE, West N, Grachan ML, Greenberg EF, Haggarty SJ, Warnow T, Mazitschek R. Nat Chem Biol. 2010 Mar;6(3):238-243. Epub 2010 Feb 7.