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.
  • American History 201

    July 21st, 2015
    Genetic studies link indigenous peoples in the Amazon and Australasia
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  • Researchers use new methods to localize genetic risk of type 1 diabetes

    July 17th, 2015

    Variation in human leukocyte antigen (HLA) genes accounts for one-half of the genetic risk in type 1 diabetes (T1D), but scientists have found it challenging to pinpoint the specific variants that account for this risk. This week, a team led by Soumya Raychaudhuri and Xinli Hu of Broad Institute and Brigham and Women’s Hospital published a study that used new genotype imputation methods to identify independent amino acid positions, as well as interactions within the HLA region, that account for T1D risk. Taking this approach, they found that three key amino acid positions in HLA-DQ and HLA-DR molecules drive the vast majority of T1D risk. To learn more, read their paper online in Nature Genetics.

  • World-leading Big Data researchers call for support for more accessible and more effective storage of data in the cloud to facilitate genomics research

    July 9th, 2015
    Improved support of cloud infrastructure is essential to the delivery of the next generation of treatments for major diseases like cancer Today in the journal Nature prominent researchers from Canada, Europe and the U.S. have made a powerful call to major funding agencies, asking them to commit to establishing a global genomic data commons in the cloud that could be easily accessed by authorized researchers worldwide.
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  • Working together against a common enemy

    July 2nd, 2015
    Public-private collaboration monitors evolution of Ebola virus
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  • Study finds no association between amylase genes, obesity

    June 30th, 2015

    The number of copies of the AMY1 gene has been reported to influence metabolic response to diet, although this locus has been difficult to study. In a recent study published in Nature Genetics, Steve McCarroll and Joel Hirschhorn of the Broad Institute and Harvard Medical School and their colleagues show that eight common sets of genetic variants, or haplotypes, almost entirely explain the number of amylase gene copies in an individual. Yet to their surprise, there was no discernible relationship between obesity and copy number. The findings offer insights that could guide future investigations of other structurally complex loci in the genome.