How clonal heterogeneity promotes metabolite exchange to support pancreatic tumors
America/Pacific Time UTC -8:00 / -7:00
Pancreatic ductaladenocarcinoma (PDA) is the third leading cause of cancer related death in the United States, contrasting a relatively low incidence rate. A principal barrier to treatment of pancreatic cancer is the densely fibrotic tumor microenvironment, where the high interstitial pressure acts to collapse blood vessels and impair the delivery of chemotherapy. This lack of functional vasculature limits nutrient availability within the tumor, causing cancer cells to develop numerous metabolic adaptations to allow for proliferation in nutrient austere conditions.
Recent studies have demonstrated several clonal behaviors of cancer cells within individual pancreatic tumors, although it is unclear if this is true of metabolism. In this webinar, Dr. Chris Halbrook, Assistant Professor at the University of California Irvine, explains how his research found the metabolic profiles of a series of clonal cell lines derived from a single tumor clustered into two distinct groups. Collectively these data demonstrate distinct metabolic classes of cancer cells within single tumors and identify asparagine as a potential target to sensitize tumors to mitochondrial inhibition.
Key learning objectives:
-Clonal heterogeneity extends to metabolism
-Cancer cell growth can be supported by metabolic crosstalk
-Asparagine supports cell proliferation when respiration is impaired
-Degradation of asparagine enhances mitochondrial inhibition
Clonal heterogeneity extends to metabolism, Cancer cell growth can be supported by metabolic crosstalk, Asparagine supports cell proliferation when respiration is impaired, Degradation of asparagine enhances mitochondrial inhibition
Previous registration necessary?
Simultaneous translation ?
Will it be recorded?