Many cancer therapies attack cellular DNA to cause DNA damage. The DNA double strand break (DSB) is the most critical form of DNA damage that induces both normal and cancer cell death if left unrepaired. My research interests involve the targeting of DNA repair pathways to enhance the therapeutic ratio. We aim to discover novel strategies to augment DNA repair pathways to specifically protect normal cells from DNA damage while reducing DNA repair capacity to convert cancer cells to become more susceptible to DNA damaging agents. Ultimately, we hope to translate our work into the clinic to deferentially treat cancer while sparing normal cells to maintain quality of life.
Keywords - nanostring, profiling, DNA damage, DNA repair, EGFR, cancer, PARP, apoptosis, brain, protection, GSK3