• Broad In Focus: Tom Green, Software Engineering Manager

    Leah Eisenstadt, April 30th, 2015

    For the past seven years, software engineering manager Tom Green has guided the development and maintenance of software tools that support the Genetic Perturbation Platform at the Broad Institute, where he can be found working with a team of software engineers or consulting with scientists conducting experimental screens. Two decades ago, however, Green was living without electricity or running water in the jungles of Nicaragua, a houseguest of locals in the remote village of Karawala on the Caribbean coast, doing a very different kind of research.

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  • Fanning the flames of lupus

    Paul Goldsmith, April 23rd, 2015

    What: A team of researchers from the Massachusetts General Hospital, Broad Institute of MIT and Harvard, and the University of North Carolina has identified an inflammatory molecule that may play an essential role in the development of lupus—a chronic, painful autoimmune disease affecting more than 1.5 million Americans.

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  • From mice to men: Broad researchers develop a human model for studying DNA methylation

    Angela Page, April 3rd, 2015

    It’s not every day that scientists get to offer their colleagues a model system that will enable a wave of future research. “Often you make a discovery, you describe it, and that’s the end of the story,” said Alexander Meissner, a Senior Associate Member at the Broad Institute of MIT and Harvard. “Here it’s not the end of something, it’s just the beginning.”

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  • Broad Summer Scholar wins prestigious Intel science prize

    Veronica Meade-Kelly, March 27th, 2015

    Each year, well over a thousand promising high school science students enter the Intel Science Talent Search, long considered the nation’s most prestigious science competition. When all is said and done, only three take home top honors and the accompanying $150,000 prize.

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  • Cancer drug resistance-from laundry list to paradigms

    Lisa Girard, March 20th, 2015

    Drug resistance is one of the greatest obstacles to effective cancer therapy. Research has shown that cancer cells can use any number of genes and strategies to achieve or acquire resistance to particular therapies. Until recently, scientists have taken a piecemeal approach to understanding the problem of resistance—unraveling individual mechanisms without reaching any kind of overarching theme.

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  • For drivers of Alzheimer’s disease, check the roadmap

    Leah Eisenstadt, March 13th, 2015

    Recently, the BroadMinded blog highlighted the exciting science emerging from the Roadmap Epigenomics program, resulting in the most comprehensive map of the human epigenome — the collection of chemical changes to DNA and its supporting proteins that help control how genes are turned on or off.

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  • Learning from Ebola

    Paul Goldsmith, March 9th, 2015

    In the fall of 2014, Ebola Zaire did for viral hemorrhagic fever what Jaws did for sharks in the summer of ‘75. The first Ebola diagnosis (and later death) on U.S. soil touched off a nationwide panic. Suddenly, Ebola was everywhere—dominating headlines, trending on social media, fueling the 24-hour news cycle. For a time, the fear and misinformation fueling the hysteria threatened to undermine relief efforts and overshadow the ongoing tragedy in West Africa.

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  • A partnership in the name of reproducible research

    Angela Page, February 27th, 2015

    In 1610, Galileo Galilei set a scientific precedent for the next half millennium: he published his notebooks. Sidereus Nuncius, as the publication was officially dubbed, documented Galilei’s observation of several astronomical features, including the orbit of Jupiter’s moons around the planet and the play of light and shadow on the earth&rsqu

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  • Epigenomics roadmap: where the road has led

    Veronica Meade-Kelly, February 20th, 2015

    The completion of the human reference genome over a decade ago served as a springboard for countless studies of genetic variation and its role in disease, but understanding how the body operates at the DNA sequence-level isn’t enough to resolve some of the finer points of human biology. Specifically: how can the same sequence of genetic code give rise to over 200 different cell types that perform distinct biological functions? And how might the processes that give rise to that functional variation contribute to human disease?

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  • Dynamic profiling of the protein life cycle in response to pathogens

    Lisa Girard, February 13th, 2015

    Cellular protein levels are dictated by the net balance of mRNA expression (the type of RNA that provides genetic information for proteins), protein synthesis, and protein degradation. While changes in protein levels are commonly inferred from measuring changes in mRNA levels (due to the difficulties involved in measuring protein levels), it’s not often clear whether determining RNA levels is actually a good proxy for measuring protein levels.

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