Research in our laboratory is focused on the responses of mammalian cells to DNA double-strand breaks (DSBs), collectively called the DNA damage response (DDR). These responses are of paramount importance in the field of cancer biology – on one hand, DSBs cause cancer, while, on the other hand, these breaks are induced by ionizing radiation or chemotherapies commonly used to treat the disease.
Our lab is involved in studying DDR events triggered by ionizing radiation – and their carcinogenic and cancer therapeutic implications.
The lab is particularly interested in understanding:
- Sensing, signaling, and repair of DSBs with an emphasis on regulation of DNA end resection, a pivotal step at which critical DSB repair decisions are made.
- Genetic basis of radio- and chemo-resistance of glioblastoma (GBM), with the translational objective of targeting DNA repair pathways to improve GBM therapy.
- Genetic changes underlying gliomagenesis triggered by ionizing radiation, the only known risk factor for the development of GBM.
A more mechanistic understanding of DDR events have emerged from these studies, providing important insights into how DSB repair and cell cycle checkpoint signaling is regulated. These studies have also led to a greater understanding of the link between genomic instability and cancer and the formulation of targeted therapeutic strategies to advance cancer treatment.