All cells acquire mutations due to cell-intrinsic and environmental exposures.  Acquired (‘somatic’) mutations have been largely cataloged in cancer, including a much smaller portion of mutations implicated in cancer development and evolution.  We and others have used mathematical approaches to identify mutational signatures – mutational imprints of cell-intrinsic and environmental mutagens – in cancer genomes, and we use them as readouts to examine mutational sources.  More recently, with advances in next-generation sequencing technologies, somatic mutations and mutational processes, some of which are implicated in cancer, have emerged as foreseeable potent contributors to an increasing number of age-related diseases beyond cancer.  However, the exact mechanisms by which many of the identified somatic mutations arise or impact physiological processes in cancer and a growing number of diseases remain poorly understood, hampering clinical translation.

Our lab investigates the mechanisms through which somatic mosaicism arises and affects the pathogenesis of cancer and other age-related diseases.  We achieve this by integrating and advancing essential computational and experimental omics approaches.  Our integrative approach aims to bridge current mechanistic gaps and, ultimately, uncover novel preventative and therapeutic strategies.

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