Bradley E. Bernstein, M.D., Ph.D.

Bradley Bernstein, M.D., Ph.D.

Chair of Cancer Biology (Dana-Farber Cancer Institute)
Richard and Nancy Lubin Family Chair (DFCI)
Professor of Pathology (HMS)
Professor of Cell Biology (HMS)
LC-8313, 450 Brookline Avenue

Bradley Bernstein, M.D., Ph.D. is the Chair of Cancer Biology at the Dana-Farber Cancer Institute, where he holds the Richard and Nancy Lubin Family Chair. He is also the Director of the Gene Regulation Observatory at the Broad Institute, a Professor of Pathology and a Professor of Cell Biology at Harvard Medical School, and an Investigator in Harvard’s Ludwig Institute.

Dr. Bernstein’s research focuses on epigenetic gene regulation. The Bernstein Lab studies how gene activity is controlled by noncoding regulatory elements such as ‘enhancers’, and by the way the genes are packaged into chromatin. His work is notable for the discovery of ‘bivalent domains’, a signature chromatin state consisting of opposing histone modifications that poise master genes for alternate fates. His characterization of bivalent chromatin and associated regulatory factors in stem cells was a key early demonstration of the mechanistic impact of chromatin on mammalian development. His subsequent work as a leader of the NIH’s ENCODE consortium revealed that the vast ‘noncoding’ portions of the human genome, which had previously been dismissed as ‘junk’, are in fact packed with sequence elements that control gene activity.

Dr. Bernstein’s second major area of contribution is cancer epigenetics. He showed that DNA methylation can activate oncogenes by disrupting genomic insulators, an entirely unexpected discovery given that methylation had been so closely tied to repression. This finding explains how certain tumors can sustain potent oncogenic signaling in the absence of canonical mutations. His group has also uncovered epigenetic mechanisms that underlie tumor cell self-renewal, drug tolerance and immune evasion.

Dr. Bernstein received his B.S. from Yale University in 1992 and his M.D. and Ph.D. from the University of Washington in 1999, before completing a residency in clinical pathology at Brigham and Women’s Hospital and postdoctoral research at Harvard University.

Dana-Farber Cancer Institute

Cancer Biology/LC-8313

450 Brookline Avenue

Boston, MA 02215

Office: 617-632-5160

Genomewide studies of histone deacetylase function in yeast.
Authors: Authors: Bernstein BE, Tong JK, Schreiber SL.
Proc Natl Acad Sci U S A
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A bullous eruption in an acutely ill child.
Authors: Authors: Strauss EA, Rao BK, Bernstein B, Scott RA.
J Cutan Med Surg
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A bisubstrate analog induces unexpected conformational changes in phosphoglycerate kinase from Trypanosoma brucei.
Authors: Authors: Bernstein BE, Williams DM, Bressi JC, Kuhn P, Gelb MH, Blackburn GM, Hol WG.
J Mol Biol
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Crystal structures of substrates and products bound to the phosphoglycerate kinase active site reveal the catalytic mechanism.
Authors: Authors: Bernstein BE, Hol WG.
Biochemistry
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A general method of domain closure is applied to phosphoglycerate kinase and the result compared with the crystal structure of a closed conformation of the enzyme.
Authors: Authors: Chandra NR, Muirhead H, Holbrook JJ, Bernstein BE, Hol WG, Sessions RB.
Proteins
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Consequences of inadequate analgesia during painful procedures in children.
Authors: Authors: Weisman SJ, Bernstein B, Schechter NL.
Arch Pediatr Adolesc Med
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The importance of dynamic light scattering in obtaining multiple crystal forms of Trypanosoma brucei PGK.
Authors: Authors: Bernstein BE, Michels PA, Kim H, Petra PH, Hol WG.
Protein Sci
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Probing the limits of the molecular replacement method: the case of Trypanosoma brucei phosphoglycerate kinase.
Authors: Authors: Bernstein BE, Hol WG.
Acta Crystallogr D Biol Crystallogr
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Synergistic effects of substrate-induced conformational changes in phosphoglycerate kinase activation.
Authors: Authors: Bernstein BE, Michels PA, Hol WG.
Nature
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Fever of unknown origin.
Authors: Authors: Miller ML, Szer I, Yogev R, Bernstein B.
Pediatr Clin North Am
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