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Assistant Professor, Pharmacology Member, Lineberger Comprehensive Cancer Center

Research Interests

  • Autophagy
  • Pancreatic cancer
  • Cancer Metabolism
  • RAS Oncogenes
  • Molecular Therapeutics

Research Synopsis

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 an anti-RAS therapeutic approach, as well as delineating other metabolic consequences of RAF-MEK-ERK MAPK inhibition. Projects will involve the use of unbiased chemical and genetic screening technologies, proteomics, confocal microscopy, and patient-tumor derived organoid culture systems. These studies will enhance our understanding of metabolic dysregulation in cancer and aid in the development of novel therapies for RAS-mutant cancers.

Motivated graduate students and post-doctoral fellows interested in joining our group are encouraged to contact me by email (


View complete list of publications in NCBI library


Kirsten Bryant, PhD