New experiments have shown how the "Seven-In-Absentia-Homolog" protein targets a key pathway for pancreatic cancer. And the research at the Mayo Clinic College of Medicine in Minnesota points to a new approach to treating the lethal disease.
Scientists already knew that a mutation in the K-RAS gene underlies the abnormal, excessive cell growth of pancreatic cancer. Because the mutated form of this growth-promoting gene is hyperactivated, a major signaling pathway that drives cell growth is in over-drive in most patients with this cancer.
The "Seven-In-Absentia-Homolog" protein seems to work as a check and balance mechanism in the K-RAS pathway by chewing up and turning off the excessive growth-promoting proteins produced by the hyperactive, mutated form of the gene, says Amy Tang whose Mayo lab conducted the research. "By attacking the SIAH-based protein-degrading machinery, we block tumor formation in one of the most aggressive human cancers cells known."
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