Researchers at NYU School of Medicine have made a key discovery that could help doctors treat one of the deadliest cancers.
A new study reveals a strategy used by pancreatic cancer cells to tinker with the immune system in a way that enables them to escape destruction by specialized immune cells.
The study, funded by the National Institutes of Health, The Pancreatic Cancer Action Network and by The Irvington Institute Postdoctoral Fellowship Program of the Cancer Research Institute, appears in the June 12 issue of Cancer Cell.
Pancreatic cancer is known for its aggressive nature. Only four percent of patients survive past five years from the time of diagnosis, and currently available therapies are largely ineffective.
"It is extremely important that we learn how the advancement of pancreatic cancer is being regulated in an effort to interrupt the progression of the disease," said senior author Dafna Bar-Sagi, PhD, senior vice president and vice dean for Science and chief scientific officer at NYU School of Medicine.
Using mouse models of pancreatic cancer, Dr. Bar-Sagi and colleagues found that a mutation of the KRAS gene, present in 95 percent of all pancreatic cancers, triggers the expression of a protein called GM-CSF. The tumor-derived GM-CSF then directs accumulation of myeloid-derived suppressor cells in the area surrounding the tumor. These cells suppress the body's natural immune defense reaction to growing tumor cells. In this way, pancreatic cancer cells escape being seen by the body's immune system and are free to grow and divide. Establishment of an immunosuppressive environment around pancreatic cancer cells, therefore, prevents their prompt rejection by the immune system.