Researchers from Duke University Medical Center and John Hopkins University School of Medicine have found that an uncontrolled cell signaling pathway that plays a vital role in the embryonic development and the liver's own response // to injury lead to the development of liver cancer.
The cell-signalling pathway called Hedgehog is present only in immature, stem-like liver cells. This discovery could lead to the development of targeted treatment of liver cancer, which happens to be one of the top causes of cancer-related deaths in the world. Jason Sicklick, M.D., a postdoctoral fellow at Duke and lead author of the study said that the researcher were able to switch off the Hedgehog pathway, which resulted in the death of the cancer cells, but spared the healthy cells that were free of cancer. "Currently, there are no good chemotherapies for liver cancer, and many people with advanced liver disease are too ill for surgery to remove tumors," Sicklick said. "There is a desperate need for effective anticancer treatments that are safe for patients with liver disease." He added that new diagnostic tests to detect cancer could also be developed in this way, "Currently, there are no good chemotherapies for liver cancer, and many people with advanced liver disease are too ill for surgery to remove tumors," Sicklick said. "There is a desperate need for effective anticancer treatments that are safe for patients with liver disease." Liver cancer is rare in people with healthy lifestyles. It is often caused in people who abuse alcohol thereby developing cirrhosis and hepatitis leading to cancer. Anna Mae Diehl, M.D., chief of Duke's gastroenterology division and senior author on the study said that the increasing incidence of obesity has meant that the risk of liver cancer has also increased, "If the liver is injured badly, it uses some of the same mechanisms to repair itself as a fetus uses in growing a liver," Diehl said. The study is to appear in the April 4, 2006,
issue of Carcinogenesis.
Becky Oskin , 919-684-4966 or 919-684-4148
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