OKLAHOMA CITY, OKLA. - New research from the University of Oklahoma reveals a previously unknown chain of events sparking the development of cancer cachexia, a debilitating muscle-wasting condition that almost always occurs in people diagnosed with pancreatic cancer.
The research, led by Min Li, Ph.D., a professor in the OU College of Medicine, is published in the journal Cancer Cell. The study is a collaboration with researchers from Johns Hopkins School of Medicine, the University of Texas Health Science Center and Yale School of Medicine.
In the study, researchers discovered that "crosstalk" between pancreatic cancer cells and macrophages (a type of immune cell) is the first step toward the onset of cachexia. Macrophages usually protect the body from infection, but in this case, the pancreatic cancer cells recruit them to do harm. Their conversation in turn prompts increased secretion of TWEAK (TNF-like weak inducer of apoptosis), a protein known to play a role in cachexia by binding to receptors on the surface of muscle cells and causing inflammation. That sequence triggers the development of cachexia.
