I am a postdoctoral research fellow in the Macara lab. My research interest is to understand the mechanism by which tissues maintain epithelial homeostasis and ways they are subverted is diseases such can cancers. Epithelia form intelligent, dynamic barriers between the external environment and an organism’s interior. The integrity of the epithelium and its proper homeostasis are of central importance to survival, and mechanism that evolved to ensure these processes are maintained during growth and in response to damage.
Indeed, the intrinsic rate of mutation in humans is an estimated 175 mutations per diploid genome per cell division. During a lifetime, humans undergo approximately 1016 cell divisions. Most of these cell divisions occur in epithelia, which is the origin of most cancers. Given this astronomical incidence, the chances that any given gene will be hit multiple times are very high. Despite there being many combinations of mutant genes that can trigger cancer, most people never develop cancer. Therefore, a fundamental question in cancer biology is why it occurs so rarely? Many mechanisms must exist to protect against cancer initiation. The underlying postulate of my work proposes that surveillance mechanisms continually assess the quality of epithelial cells in tissues such as breast, and eliminate defective (and pro-cancerous) cells by inducing apoptosis. We propose that this mechanism protects against the initiation of breast cancers caused by loss of normal epithelial polarity and that suppression of apoptosis together with loss of polarity is an early event in many cancers.
My clinical mentor is Dr. Brent Rexer who is an oncologist with specialty in breast cancer. His expertise provides me with the clinical perspectives on the disease and help adapt my research in ways so it is clinically relevant.