Our research program uses innovative genetic and genomic approaches, using both Sleeping Beauty transposon mutagenesis data from mouse cancer models and somatic mutation data from human cancer genomes, to discover the genetic and epigenetic events that initiate, progress, and contribute to acquired therapeutic resistance during the evolution of melanoma and non-melanoma skin cancers.
Cancer driver discovery continues to advance research with the promise of identifying genetic and epigenetic determinants that may contribute to new diagnostic markers and targeted therapeutics. The overarching goal of our research program is to define the functions of cancer drivers in the pathogenesis of skin cancer. Our Cutaneous Cancer Driver Discovery Program (C2D2P) is currently focused on defining cooperating mutational events that drive normal melanocyte transformation to cutaneous Melanoma (cuMEL) and normal keratinocyte transformation to cutaneous Squamous Cell Carcinoma (cuSCC). We use a high-throughput mouse modeling platform and human cell culture models to functionally validate co-mutated drivers that propel initiation and progression of cuMEL and cuSCC. Future efforts will be centered on the creation of a new generation of pre-clinical mouse models to probe in vivo drug resistance mechanisms and therapeutic target gene/pathway selection with demonstrated biological importance and translational application. Applying this information in the context of human cancer will advance cutaneous oncology research.