The proposed Broad Institute Center for Cancer Systems Biology represents a multi-investigator effort that has several concrete goals. First, we aim to create and maintain a vibrant community of cancer biologists and computational scientists devoted to exploring the emerging field of cancer systems biology. This will involve maintaining a rich intellectual environment that rigorously develops new, and highly integrated experimental and computational approaches to cancer research. This will involve training a next generation of cancer researchers who become increasingly expert at this cancer biology / computational biology interface, through the development and dissemination of computational tools (software), cross-disciplinary training, and multimedia educational materials. In addition, the Center will take on an ambitious, multiinvestigator research project aimed at identifying the essential genes (Achilles'Heels) of cancers of different types, and developing advanced computational models that use the molecular features of cancer cells to predict these essentialities. If successful, this effort would yield both new insights into the molecular circuitry of cancer cells, and would also provide a new path towards personalized cancer medicine, whereby the molecular features of a patient's tumor are predictive of their response to specific therapy.
The proposed Center holds great potential to yield both new insights into the molecular circuitry of cancer cells, and provide a new path towards personalized cancer medicine, whereby the molecular features of a patient's tumor are predictive of their response to specific therapy. In addition, the Center will serve as a training ground for a next generation of researchers of cancer systems biology.
|Geller, Leore T; Barzily-Rokni, Michal; Danino, Tal et al. (2017) Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine. Science 357:1156-1160|
|Okondo, Marian C; Johnson, Darren C; Sridharan, Ramya et al. (2017) DPP8 and DPP9 inhibition induces pro-caspase-1-dependent monocyte and macrophage pyroptosis. Nat Chem Biol 13:46-53|
|Tsherniak, Aviad; Vazquez, Francisca; Montgomery, Phil G et al. (2017) Defining a Cancer Dependency Map. Cell 170:564-576.e16|
|Ilic, Nina; Birsoy, K?vanç; Aguirre, Andrew J et al. (2017) PIK3CA mutant tumors depend on oxoglutarate dehydrogenase. Proc Natl Acad Sci U S A 114:E3434-E3443|
|Godec, Jernej; Tan, Yan; Liberzon, Arthur et al. (2016) Compendium of Immune Signatures Identifies Conserved and Species-Specific Biology in Response to Inflammation. Immunity 44:194-206|
|Kryukov, Gregory V; Wilson, Frederick H; Ruth, Jason R et al. (2016) MTAP deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in cancer cells. Science 351:1214-8|
|Zhu, Xiaodong; Girardo, David; Govek, Eve-Ellen et al. (2016) Role of Tet1/3 Genes and Chromatin Remodeling Genes in Cerebellar Circuit Formation. Neuron 89:100-12|
|Yu, Channing; Mannan, Aristotle M; Yvone, Griselda Metta et al. (2016) High-throughput identification of genotype-specific cancer vulnerabilities in mixtures of barcoded tumor cell lines. Nat Biotechnol 34:419-23|
|Tirosh, Itay; Izar, Benjamin; Prakadan, Sanjay M et al. (2016) Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq. Science 352:189-96|
|Liberzon, Arthur; Birger, Chet; Thorvaldsdóttir, Helga et al. (2015) The Molecular Signatures Database (MSigDB) hallmark gene set collection. Cell Syst 1:417-425|
Showing the most recent 10 out of 41 publications