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Bradley E. Bernstein, MD, PhD

Professor, Department of Pathology, Harvard Medical School

Associate Pathologist, Pathology, Massachusetts General Hospital

Contact Info

Bradley Bernstein
Massachusetts General Hospital
Molecular Pathology

Boston, MA, 02114
Phone: 617-726-6906
Fax: 617-643-3566
bernstein.bradley@mgh.harvard.edu

Assistant

Julie Finn
Administrative assistant
Massachusetts General Hospital
Phone: 617-643-3559
jmfinn@MGH.harvard.edu

DF/HCC Program Affiliation

Cancer Genetics

Research Abstract

Associate Professor of Pathology at Harvard Medical School, an Early Career Scientist at Howard Hughes Medical Institute and an Associate Member at the Broad Institute. Laboratory in the Richard B. Simches Research Building at Massachusetts General Hospital, part of Experimental Pathology and the Center of Systems Biology with research focused on chromatin and epigenetic regulation in normal and malignant stem cells. The laboratory applies high-throughput sequencing-based technologies to characterize chromatin structure and DNA methylation genome-wide in human and mouse cells. In addition to advancing technology and providing unprecedented global views of mammalian chromatin, this work has led to an appreciation of the role of large-scale chromatin structures, or ‘domains’, in regulating developmental genes. For example, in differentiated cells, chromatin domains marked by either ‘active’ or ‘repressive’ histone modifications maintain expression or repression of key developmental genes. However, in pluripotent ES cells, chromatin domains enriched for both active and repressive modifications repress developmental genes while maintaining their potential for subsequent activation. Current projects in the lab are focused on these 'bivalent' domains with the goals of understanding their initial establishment, their higher-order structure, and their roles in ES cell pluripotency and epigenetic regulation of development. Similar approaches are also being used to characterize chromatin modifications in adult stem cells and cancer models. In particular, recent work has shed light on the epigenetic and transcriptional regulatory networks in Wilms tumor and Glioblastoma.

Publications

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