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 approach models NAHR abnormalities

    February 14th, 2016

    Genetic disorders are often hard to model. This is particularly true for those caused by non-allelic homologous recombinations (NAHR) — which occur when highly similar portions of the genome wrongly recombine. A new study from Broad associate members James Gusella and Michael Talkowski, both of Massachusetts General Hospital (MGH) and Harvard Medical School (HMS), and first author Derek J.C. Tai, also of MGH and HMS, describes a new method for using the genome engineering tool CRISPR/Cas-9 that accurately models NAHR abnormalities. Find out more about this new approach and what it means for the study of genetic disorders in Nature Neuroscience.

  • Broad Institute founding director Eric S. Lander receives the 2015 Abelson Prize

    February 11th, 2016
    The American Association for the Advancement of Science (AAAS) honors Eric Lander with Abelson Prize for "work bringing science to bear in serving the public’”
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  • New HDAC inhibitor toolkit helps reveal potential therapy to protect pancreatic β-cells from effects of diabetes

    February 2nd, 2016

    Histone deacetylase inhibitors (HDACi) hold therapeutic potential for many diverse diseases, including psychiatric disease and diabetes. But so far, most HDACi were found to inhibit more than one histone deacetylase, a characteristic that can decrease efficacy and contribute to side effects. In work published in ACS Chemical Biology, researchers Edward Holson and Florence Wagner of the Broad’s Stanley Center for Psychiatric Research, and colleagues present a toolkit of highly potent and differentially selective HDACi, which they developed to understand the role of histone deacetylases in cognition. The paper also reports the results of a collaboration with Bridget Wagner of Broad’s Center for the Science of Therapeutics, who used the toolkit to reveal that the isoform selective inhibition of HDAC3 by BRD3308 protects pancreatic beta cells from the effects of diabetes.

  • First glimpse of schizophrenia’s genetic roots shines light on a developmental process gone awry

    January 26th, 2016
    Groundbreaking work is the result of analytical ingenuity, fortuitous collaborations, and catalytic philanthropic funding
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  • Genetic study provides first-ever insight into biological origin of schizophrenia

    January 26th, 2016
    Landmark analysis reveals excessive “pruning” of connections between neurons in brain predisposes to schizophrenia
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