Steven D. Cappell, PhD, with his sponsor Tobias Meyer, PhD, at Stanford University, Stanford, California, aims to understand the precise molecular events that allow cells to enter the cell cycle (process of cell division), by applying quantitative time-lapse microscopy, live-cell fluorescent reporters and mathematical modeling. The beginning of the cell cycle, the G1/S phase transition, represents the commitment to cell division and is deregulated in nearly all types of cancers. He hopes to identify new regulatory elements controlling the G1/S transition that can be targeted for therapeutic benefit.
Elie J. Diner, PhD, with his sponsor Russell E. Vance, PhD, at the University of California, Berkeley, California, seeks to understand how the innate immune system distinguishes between self- and non-self nucleic acids. This research has a direct application to cancer and tumor biology, as cancerous cells undergo uninhibited cell growth that typically remains undetected by the immune system. Understanding how the immune system recognizes or avoids recognition of specific molecules may lead to the discovery of pathways that can be exploited to direct the immune system to target tumor cells.
Damian C. Ekiert, PhD, with his sponsor Jeffery S. Cox, PhD, at the University of California, San Francisco, California, is exploring the complex network of interactions between the host immune system and Mycobacterium tuberculosis, the pathogen that causes tuberculosis (TB) in humans. In order to survive and replicate inside host cells, M. tuberculosis must evade detection by the immune system and interfere with multiple antimicrobial pathways that would otherwise lead to the destruction of the bacteria. Understanding how pathogens escape immune recognition may shed light on how cancerous cells evade detection by similar tissue surveillance mechanisms.
|Contact: Yung S. Lie, Ph.D.|
Damon Runyon Cancer Research Foundation