{"id":5,"date":"2017-06-21T15:13:49","date_gmt":"2017-06-21T15:13:49","guid":{"rendered":"https:\/\/med-template.sites.unc.edu\/home\/"},"modified":"2022-07-06T12:52:33","modified_gmt":"2022-07-06T16:52:33","slug":"home","status":"publish","type":"page","link":"https:\/\/www.med.unc.edu\/pharm\/bryantlab\/","title":{"rendered":"Home"},"content":{"rendered":"

\"iagram<\/p>\n

The overall goal of our lab is to perform research that contributes to a better understanding of pancreatic cancer biology and leads to improved treatments for this disease. One major focus of our studies is the metabolic activity, autophagy, which is a self-degradation process whereby cells can orderly clear defective organelles and recycle macromolecules as a nutrient source. Autophagy is elevated and essential for the tumorigenic growth of KRAS-mutant pancreatic ductal adenocarcinoma (PDAC). We recently determined that the treatment of PDAC with inhibitors of the key KRAS effector pathway, the RAF-MEK-ERK mitogenic activated protein kinase (MAPK) cascade, caused further elevation of autophagy, rendering PDAC acutely dependent on this process, and hypersensitive to autophagy inhibition. Current projects are focused on further advancing autophagy inhibition as a therapeutic approach, as well as delineating other metabolic consequences of RAF-MEK-ERK MAPK inhibition.<\/p>\n

Work in the Bryant Lab is generously funded by:<\/p>\n