"MAOA expression variability: pathways and risks in Prostate Cancer."
I am studying the relevance of monoamine oxidase A (MAOA) in prostate cancer (PCa) by integrating mechanistic molecular studies with population-based epidemiologic analyses. MAOA activity generates ROS as well as deaminated products that promote proliferation and therefore may contribute to PCa progression. The Nelson lab has shown an association between poor response to chemotherapy and elevated MAOA expression in prostate epithelium, and found in vitro that MAOIs (MAOA inhibitors used clinically for depression) reduced cell viability and, when coupled with docetaxel, enhanced apoptosis and improved responses to chemotherapy. MAOA may also contribute to PCa progression by interfering with hormone receptor-mediated regulation. Such a finding could shed light on mechanisms of androgen sensitivity and influence aggressive phenotypes in a variety of cancers. I am pursuing these lines of inquiry at the bench, and will leverage our findings to undertake epidemiologic investigations with translational potential using existing longitudinal studies created by the Stanford group. For example, I will evaluate whether exposures such as common genetic polymorphisms of MAOA, or MAOI use, are associated with differential risk of PCa incidence or outcomes.