Scientists at the Johns Hopkins Kimmel Cancer Center have identified a molecular partnership in pancreatic cancer cells that might help to explain how the disease spreads (metastasizes) in some cases. Their findings reveal urgently needed new targets to treat pancreatic cancer, which strikes nearly 50,000 people in the U.S. each year and has only a 5 percent survival rate five years after diagnosis. One of the molecular partners is annexin A2, a protein that scientists say was already linked to poor survival rates in these cancers. In a report published in the August 4, 2015 issue of Science Signaling, Lei Zheng, M.D., Ph.D., and his colleagues show that annexin A2 helps usher a protein called semaphorin 3D (Sema3D) out of pancreatic cancer cells. Once outside the cells, Sema3D joins with another molecule (plexin D1) to fuel the cancer's spread. The new article is titled “Semaphorin 3D Autocrine Signaling Mediates the Metastatic role of *Annexin A2 in Pancreatic Cancer.: Sema3D is a protein that guides the projecting arms of nerve cells, called axons, as the nerve cells grow and develop. In experiments with mice, the researchers calculated a seventy-fold drop in the amount of Sema3D secreted from mouse pancreatic cancer cells in animals that lacked annexin A2. In an experiment involving 23 mice, none of the annexin-free animals developed visible metastatic tumors. By contrast, 16 out of 17 mice that produced annexin A2 in their cells developed metastatic tumors in the liver, lungs or abdominal cavity. In a second group of experiments using human tissue from patients with pancreatic ductal adenocarcinoma, which accounts for more than 90 percent of pancreatic cancers, Dr.
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