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Hunter Li
Ph.D. Program
Previous Degree: B.Sc. Biology

2010 Cohort

Tumors are often associated with defective DNA damage response (DDR) pathways and increased chromosome instability (CIN). Many anti-cancer therapeutics exploit defects in the DDR by generating DNA damage that can in turn result in cell death. In my graduate research in the Hieter Lab, Saccharomyces cerevisiae is used as model organism to investigate the efficacy of targeting DNA repair enzymes in cancer-associated genetic backgrounds together with treatment by genotoxic agents. We hypothesize that knockdown of these repair enzymes will sensitize certain genetic backgrounds to selective cytotoxic killing by DNA damaging agents resulting in synthetic cytotoxicity. In this proof of principle study, we will assess the feasibility of using high throughput genetic methods in yeast to discover synthetic cytotoxicity relationships between repair enzyme inhibitors, DNA damage chemotherapeutic agents, and somatic mutations found in tumors. The data derived in model organisms would provide the basis for expanding the screening paradigm, and for testing specific combination therapies for selective killing of cultured cancer cells.

Supervisor: Philip Hieter