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.
  • Remembering Ted Stanley

    January 11th, 2016
    His commitment has changed the study of psychiatric disease into a molecular field based on rigorous analysis of the action of specific genes and proteins
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  • Team builds hallmark gene set collection from Molecular Signatures Database

    January 11th, 2016

    A team led by Pablo Tamayo and Jill Mesirov of the Broad Institute and University of California, San Diego, and Broad bioinformatician Arthur Liberzon, has generated “hallmark” gene sets from the Molecular Signatures Database (MSigDB), one of the most comprehensive and widely used databases for gene set enrichment analysis. Through both automated and manual approaches, the team curated a refined collection of MSigDB gene sets that reduce redundancy and produce more robust analyses. Their paper is published in Cell Systems.

  • Genome misfolding unearthed as new path to cancer

    December 23rd, 2015
    IDH mutations disrupt how the genome folds, bringing together disparate genes and regulatory controls to spur cancer growth
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  • Super-enhancers, amplified: Study of noncoding genome regions suggests common mechanism activating cancer driver genes

    December 22nd, 2015

    In a new paper published online by Nature Genetics, researchers from Dana-Farber Cancer Institute (DFCI) and the Broad Institute systematically investigated somatic copy number alterations of noncoding regions across cancers, integrating genomic, epigenomic, and transcriptomic data.

    The team found six super-enhancer regions that are focally amplified across different cancer types, including two that are associated with overexpression of the MYC oncogene, suggesting that this type of modification may be a common mechanism activating cancer driver genes. The team, which was led by senior author Matthew Meyerson and first authors Xiaoyang Zhang, Peter Choi, and Joshua Francis – all of Broad and DFCI – also used genome-editing technologies to validate the oncogenic function of these focally amplified super-enhancers.

  • Study explores mutation’s paradoxical role in myeoloproliferative neoplasms

    December 20th, 2015

    Myeloproliferative neoplasms (MPNs) are a series of blood disorders that tend to lead to acute myeloid leukemia (AML). The most common genetic mutation in MPNs is called JAK2V617F, an activating mutation in JAK2 kinase. Although JAK2V617F has been associated with increased DNA damage, MPNs are diseases characterized by genomic stability.

    In a recent paper published by Cell Reports, Broad associate member and senior author Ann Mullally, first author Edwin Chen, and colleagues address this paradox by showing that a DNA helicase called RECQL5 suppresses genomic instability in MPNs even as JAK2V617F instigates a state of DNA damage.