Genetic instability is a hallmark of cancer.
Our lab has focused on the molecular mechanisms of common types of genetic rearrangements and the genes which are mutated in normal cells to allow them to arise. Chromosome breakage is centrally involved in gene amplification, deletions, and translocations. We showed that mutations in cell cycle control genes such as p53 greatly reduce genetic stability. Importantly, p53 is the most commonly mutated gene in human cancers. Part of our research efforts are directed at understanding how different stresses activate p53 and how they lead to gene expression programs that produce effects ranging from cell cycle arrest to cell death.