Due to their rapid metastatic spread, pancreatic tumors are among the most aggressive types of cancer. Only three to five percent of patients have a survival rate of five years. A team of researchers at the Karlshue Institute of Technology (KIT) in Germany has now established a basis for new therapeutic approaches In an article published online on October 24, 2015 in Gastroenterology, the scientist report that in various pancreatic cancer mouse models CD44v6-specific peptides do not only inhibit the spread of tumor cells, but may even lead to the regression of already existing metastases.The article is titled “Inhibition of Tumor Growth and Metastasis in Pancreatic Cancer Models by Interference with CD44v6 Signaling.” “We think that these peptides have a high potential for tumor therapy, above all for the treatment of pancreatic cancer with its aggressive metastases,” Véronique Orian-Rousseau, Ph.D., Group Leader in the Institute of Toxicology and Genetics (ITG) at KIT, says. The CD44v6 protein was discovered in the 1990s by KIT researchers. It acts as a co-receptor for receptor tyrosine kinases, such as MET or VEGFR-2, that depend on CD44 for their activation. These enzymes largely influence the activities of tumor cells. MET accelerates their proliferation, migration, and invasion. VEGFR-2 promotes angiogenesis, i.e., the formation of new blood vessels required to supply the tumor. Hence, MET and VEGFR-2 are decisive for the growth and spread of tumor cells. In pre-clinical studies on animals and using various pancreatic cancer models, KIT scientists have proved, for the first time, that the co-receptor function of CD44v6 drives the metastatic spreading. Interestingly, small segments of the CD44v6 protein (called v6pep) turned out to be successful inhibitors of metastasis in animal experiments.
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