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Cancers are driven by genomic and epigenetic alterations that result in the activation of cellular proto-oncogenes and the inactivation of tumor suppressor genes. Although high-throughput genomic approaches have begun to establish extensive catalogs of gene alterations in human tumors, the genes that control tumor genesis, progression, and response to therapies are often concealed by the complex chromosomal instability in cancer cell genomes. This challenge is exacerbated by the lack of functional annotation for the vast majority of genes in the human genome.