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.
  • Illuminating the broad spectrum of disease

    February 29th, 2016
    PRISM efficiently tests drug compounds in multiple cell lines simultaneously, accelerating discovery of targeted therapies in the service of precision medicine
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  • Haptoglobin variation: new insights into roots and role

    February 26th, 2016

    One of the first protein polymorphisms identified in humans involves alternative forms of haptoglobin, one of the most abundant proteins in the blood. The genetic origins and medical significance of this variation have puzzled scientists since its discovery. Now, a team of researchers from the Broad Institute’s Medical and Population Genetics Program led by institute member Steve McCarroll and postdoctoral associate Linda Boettger has revealed that haptoglobin variation likely arose from the combined effects of many deletions among human ancestors. The study, published this week in Nature Genetics, goes on to find that these deletions contribute to lower blood cholesterol levels. The findings may also represent an interesting example of exon deletions that exert a beneficial effect on protein structure and human health.

  • Restoration of Shank3 gene activity in adult mice aids recovery from some neurodevelopmental deficits, but not others

    February 17th, 2016

    A longstanding question in neurodevelopmental biology has been whether, or to what degree, traits resulting from neurodevelopmental disorders might be reversible.

    In a study published this week in Nature, a team led by Guoping Feng of the McGovern Institute for Brain Research at MIT and the Stanley Center for Psychiatric Research at Broad Institute, McGovern’s Yuan Mei, and Broad’s Patricia Monteiro, looked at mice born with impairments to Shank3, a gene known to contribute to a subset of autism cases. By reactivating the gene at different times of development, the researchers found that certain behavioral abnormalities caused by the impairment to Shank3, such as social deficits and repetitive behaviors, could be rescued even in adulthood, while other traits, such as anxiety and motor coordination deficits, could only be rescued early in development. The findings inform our understanding of brain plasticity and suggest that therapeutic interventions for neurodevelopmental disorders may be more effective if delivered early in development. Read more about their findings in MIT News.

  • 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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