News from the Broad

The Broad Institute is committed to open sharing not only of its scientific data and tools, but also information and news about our progress towards achieving our mission. Below are just a few highlights from the Broad scientific community.
  • New study examines cell survival in low-oxygen tumor environments

    April 13th, 2015

    How do cancer cells survive the low blood supply of the tumor microenvironment? A team led by Broad senior associate member David Sabatini, a member of the Whitehead Institute for Biomedical Research and professor of biology at MIT, recently found that brain cancer cells express high levels of metabolic enzymes SHMT2 and GLDC, and the resulting reduced oxygen consumption gives the cells a survival advantage in poorly vascularized tumor regions. Inhibiting GLDC in SHMT2-overexpressing cells leads to toxic glycine accumulation and may be a possible new avenue for therapeutics. The study was published online by the journal Nature.

  • Broad Institute-MIT team identifies highly efficient new Cas9 for in vivo genome editing

    April 1st, 2015
    New finding is expected to expand therapeutic and experimental applications of CRISPR
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  • Broad Institute of MIT and Harvard and Bayer Healthcare expand their partnership to develop therapies for cardiovascular disease

    March 31st, 2015
    The Broad Institute of MIT and Harvard have expanded their collaboration with Bayer HealthCare to include cardiovascular genomics and drug discovery. The goal of this new part of the alliance is to leverage insights from human genetics to help create new cardiovascular therapies.
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  • Findings help unravel lung cancer drug resistance

    March 18th, 2015

    One of the primary limitations to the effectiveness of cancer therapeutics is drug resistance. This month in the journal Cell, Broad researchers Rick Wilson, Levi Garraway, and colleagues describe their work unraveling drug resistance mechanisms for ALK tyrosine kinase inhibitors in ALK-dependent non-small cell lung cancers. They screened nearly 16,000 ORFs corresponding to over 12,000 genes, identifying a range of known mechanisms able to confer resistance to ALK inhibitors, along with new ones including purinergic P2Y receptors (G-protein coupled receptors) acting through Protein Kinase C signaling.

  • Broad Institute and Calico announce an extensive collaboration focused on the biology of aging and therapeutic approaches to diseases of aging

    March 17th, 2015
    The Broad Institute of MIT and Harvard has entered into a partnership with Calico around the biology and genetics of aging and early-stage drug discovery. The partnership will support several efforts at the Broad to advance the understanding of age-related diseases and to propel the translation of these findings into new therapeutics.
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