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ӳý of MIT and Harvard today announced a $10 million gift from the Gerstner Family Foundation that will expand cancer research at ӳý and broaden collaborations with Dana-Farber/Harvard Cancer Center and Memorial Sloan Kettering Cancer Center. The research will focus on the changes tumors undergo as they become resistant to drugs, which is the biggest hurdle to conquering the disease.

Fetal hemoglobin, which is normally replaced by adult hemoglobin a few months after birth, can ameliorate symptoms of beta-thalassemia and sickle cell anemia. Boosting fetal hemoglobin by inhibiting the transcription factor BCL11A holds therapeutic promise, but BCL11A's role in the body isn’t fully understood. To study its in vivo effects, a team led by ӳý associate member Vijay Sankaran, Mark Daly, co-director of the ӳý’s Medical and Population Genetics Program, and Zdenek Sedlacek of University Hospital Motol (Czech Republic) identified and characterized three patients with an autism spectrum disorder and developmental delay who harbored deletions of the BCL11A gene. , appearing in the Journal of Clinical Investigation, provides evidence of BCL11A’s role in neurodevelopment and suggests caution when developing BCL11A-targeting therapies.

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The started five years ago with the goal of creating a comprehensive atlas and open database of gene expression and gene regulation across human tissues. This week, the researchers spearheading the NIH-funded effort reporting on the pilot phase of the project.

GTEx

Researchers funded by the National Institutes of Health Genotype-Tissue Expression (GTEx) project, including scientists from the ӳý of MIT and Harvard, have created a new and much-anticipated data resource to help establish how differences in an individual’s genomic make-up can affect gene activity and contribute to disease. The new resource will enable scientists to examine the underlying genomics of many different human tissues and cells at the same time, and promises to open new avenues to the study and understanding of human biology.