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.
  • Tool for annotating cancer-related variants now publicly available

    May 5th, 2015

    Cancer genome sequencing can reveal thousands of mutations per tumor, but scientists need more data to interpret those variants. Since 2011, members of Broad's Cancer Genome Analysis team have used Oncotator, a tool for annotating cancer-related variants, resulting in more than 20 publications. In the journal Human Mutation, a team led by Broad researchers Gad Getz, Alex Ramos, and Lee Lichtenstein announced the first public release of Oncotator, which draws information from 14 publicly available cancer resources and is available as a python module hosted on Github, as well as a web service and stand-alone application.

  • New MCL1 protein construct solves previously intractable structural biology problem

    May 4th, 2015

    As one of the most commonly altered genes in cancer, MCL1 has been the focus of widespread drug development efforts — but the gene, which encodes a protein that helps keep cells alive, remains an elusive target. A new finding published this week by Broad researchers is expected to catalyze the development of effective MCL1 inhibitors. The team, led by senior author Michael Serrano-Wu, designed a new MCL1 protein construct that provides a robust solution to a previously intractable structural biology problem. Their paper is published online in PLoS One.

  • Better data for the bedside: Broad sequencing gets closer to the clinic

    May 1st, 2015
    CRSP appoints a new clinical director and aims to increase the impact of clinical sequencing services
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  • Study identifies mechanism by which hydroxamate-based HDAC inhibitors protect neurons from oxidative stress

    April 30th, 2015

    The development of histone deacetylase inhibitors to treat a variety of diseases has been somewhat hampered by HDAC-related toxicity concerns. A team from the Stanley Center for Psychiatric Research at Broad Institute, led by the Center’s director of medicinal chemistry Ed Holson and Broad postdoctoral associate David Olson, has discovered a new HDAC-independent mechanism by which some hydroxamate-based HDAC inhibitors protect neurons from oxidative stress, such as during stroke.

  • Fine mapping of MHC region leads to identification of new genetic risk factors for celiac disease

    April 29th, 2015

    In a study published online last week in Nature Genetics, a team led by Broad visiting scientist Paul de Bakker of University Medical Center Utrecht fine mapped the major histocompatibility complex (MHC) – a linked set of genetic loci known to influence the development of celiac disease. The team’s approach turned up five new associated genetic variants that together account for roughly 18% of the genetic risk for the disease. Combined with previously identified risk factors, these genetic loci can now explain up to 48% of celiac disease heritability.