Ph.D. Baylor College of Medicine Post-doc:Columbia University
Genome stability is maintained by intricate networks of cell cycle checkpoint proteins. In response to genotoxic stress, either extrinsic such as ionizing radiation-induced DNA breaks or intrinsic such as oxidative damage, a cascade of signaling events are initiated to arrest the cell cycle, eliminate damaged cells, or to repair the damage. Defects in these responses often lead to accumulation of mutations and development of cancers. Our studies are focused on targets of the checkpoint pathways involving the tumor suppressors and the checkpoint kinases CHK1 and CHK2, of which mutations are associated with human cancers. Our main goals are to decipher the molecular basis of checkpoint control by these proteins, their functional relationship with DNA repair and genome maintenance, and the impacts on tumorigenesis. By using molecular approaches, cell-based and mouse models, we hope to uncover novel tumor suppressors and their modes of action, through which potential therapeutics could be devised to improve cancer treatment.
JAK2-CHK2 signaling safeguards the integrity of the mitotic spindle assembly checkpoint and genome stabilityCell Death & Disease, Jul 18, 2022
Loss of the tumor suppressor BTG3 drives a pro-angiogenic tumor microenvironment through HIF-1 activationCell Death & Disease, Dec 11, 2020