E. Alejandro Sweet-Cordero, MD
The goal of my laboratory is to identify novel therapeutic approaches for cancer that target the genetic mutations and altered signaling networks that are specific to cancer cells. We use functional genomics applied to mouse and human systems (genetically engineered models, patient derived xenografts) to understand the transcriptional networks that regulate the outcome of specific oncogenic mutations and to understand how cancers become resistant to chemotherapy. We have two primary disease interests: lung cancer and pediatric sarcomas. Our laboratory has identified novel regulators of chemoresistance in lung cancer (Oliver et al, 2010 Genes and Development). We have used functional genomics in mouse and human models to identify a novel role for Wt1 in mediating KRAS-driven oncogenesis (Vicent et al, 2010, JCI). We have identified and characterized the role of tumor-propagating cells in NSCLC and identified a key role for Notch3 as a self-renewal pathway in mouse and human NSCLC (Zheng et al, 2013, Cancer Cell). In our sarcoma work, we are interested in mechanisms driving osteosarcoma and Ewing sarcoma progression. We recently identified the first lncRNA involved in the pathogenesis of Ewing sarcoma (Howarth et al, JCI, 2014). We rely heavily on computational genomic analysis in our work and we have extensive experience in generating and using high-throughput datasets and next-generation sequencing for gene and network discovery. We are also actively involved in a multidisciplinary effort to apply next-generation sequencing (WGS/RNAseq etc) to advance the care of relapsed and other high-risk pediatric cancer patients at UCSF/Benioff Children’s Hospitals.