Bradley Bernstein, MD, PhD
Massachusetts General Hospital
Associate Professor of Pathology
Harvard Medical School
Early Career Scientist
Howard Hughes Medical Institute
Senior associate Member, Broad Institute
The long-term goal of our research is to achieve a comprehensive understanding of chromatin structure and function in mammalian development and human cancer. We are taking a multi-faceted approach involving stem cell biology, genetics, genomics and computational biology. Considerable efforts are being directed towards the development and application of emerging technologies for genomewide analysis of chromatin across diverse cell lineages, with the goal of deciphering the nature and function of the ‘mammalian epigenome’. These studies have led to several discoveries, including the identification of bivalent domains, a novel chromatin structure proposed to keep developmental regulator genes ‘poised’ in pluripotent ES cells.
Current studies are applying stem cell biology and functional tools to characterize the functions of bivalent domains and associated chromatin regulators, such as Polycomb and trithorax complexes. We broadly hypothesize that these chromatin associated proteins play critical roles in balancing potency and lineage-commitment, and guiding lineage decisions throughout development. Recent studies have begun to apply the emerging technologies and computational methods to characterize the chromatin landscapes of malignant cells, with the goal of understanding how epigenetic deregulation can contribute to human cancer.
Members of the Laboratory
Current projects in the lab are focused on the 'bivalent' domains with the goals of understanding their initial establishment, their higher-order structure, and their roles in ES cell pluripotency and epigenetic regulation. Similar approaches are also being used to characterize chromatin modifications in adult stem cells and cancer models. Our long-term goal is to achieve a systems level understanding of chromatin regulation during development, and how chromatin mis-regulation contributes to human disease.
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