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Research in the News
Grant recipient reveals an unexpected energy source for pancreatic tumors
A compelling study conducted by a Pancreatic Cancer Action Network research grant recipient was recently published online in the prominent scientific journal Nature. Cosimo Commisso, PhD received the Fellowship Award from the Pancreatic Cancer Action Network in 2011, funded in memory of Samuel Stroum. He is a postdoctoral fellow in the laboratory of Dafna Bar-Sagi, PhD, recipient of a 2008 Pancreatic Cancer Action Network Pilot Grant and co-principal investigator of the inaugural 2013 Research Acceleration Network grant funded by Tempur-Pedic in memory of Tim Miller. Dr. Bar-Sagi is also a member of our Scientific Advisory Board, along with a collaborator on the study, Craig Thompson, MD.
The theme of the Nature paper relates directly to Dr. Commisso’s project that was funded by our organization, and Pancreatic Cancer Action Network is cited among the funding sources that allowed the research to take place. Dr. Commisso and colleagues evaluated the role of a process called macropinocytosis in the growth and progression of pancreatic tumors. Macropinocytosis allows cells to take in large quantities of fluid that is present outside the cell (known as extracellular fluid). Since there are nutrients present in the extracellular fluid, macropinocytosis is a way for cells to take in sources of nourishment and energy.
One of the major components of the extracellular fluid is the protein albumin. Albumin is a particularly rich source of the amino acid (protein building block) glutamine, and pancreatic cancer cells are known to be dependent on glutamine for growth and survival. Dr. Commisso and the research team used different mouse models of pancreatic cancer to study macropinocytosis, and found that this process is dependent on mutant K-Ras. Over 90 percent of pancreatic tumors are known to express and rely on mutant, hyperactive K-Ras. Since mutant K-Ras activity cannot be directly blocked, Dr. Commisso and colleagues studied the repercussions of blocking macropinocytosis. Encouragingly, preliminary experiments in the mice suggest that inhibiting macropinocytosis could be a means to starve the pancreatic cancer cells, and thus stop or slow their growth, without significantly harming normal cells.
Future studies will be necessary to further understand the interdependence between mutant K-Ras activity, macropinocytosis, and the progression of pancreatic cancer.
