Scientists at Cold Spring Harbor Laboratory (CSHL) have taken the search for cancer-causing genes an important step forward. In a newly published paper, they confirm that a gene called DLC1 is a tumor suppressor. They have demonstrated in living mice that its deletion, inactivation or loss precipitates events culminating in an aggressive type of liver cancer closely related to common human epithelial cancers of the liver (also known as hepatocellular carcinoma, or HCC).
The team's success in tracing the intricate pathway by which DLC1 functions in both healthy and pathological states suggests a highly specific new target for future anticancer drugs.
Focusing on a Suspected Tumor Suppressor Tumor suppressor genes play a vital role in intracellular signaling networks that protect against uncontrolled cell growth and proliferation. Such genes can be rendered inactive by a variety of DNA alterations, including deletions, mutations and so-called epigenetic changes in DNA's chemical configuration. DLC1 a gene whose acronym reflects prior suspicions that it was "deleted in liver cancer" was known to be located in a region of chromosome 8 that has been observed to be missing in past studies of mammalian liver cancer cells. "The region in question is a large one that may harbor more than one tumor suppressor," said Dr. Scott W. Lowe. "We set out to conclusively identify DLC1 as a tumor suppressor, which had not been done before, and to show at the molecular level how the absence of this gene produces pathology in cells that can lead to liver cancer. Interestingly, loss of DLC1 is observed in a range of epithelial cancers, which suggests that DLC1 may a play common role in many types of human cancer."
In addition to corresponding author Lowe, the research team included five other laboratory heads at CSHL: Prof. Linda Van Aelst, Ph.D., and Prof. Michael Wigler, Ph.D.; Assoc. Prof. Scott Powers, Ph.D.; and Asst. Prof. Robert Lucito, Ph
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| Contact: Jim Bono bono@cshl.edu 516-367-8455 Cold Spring Harbor Laboratory Source:Eurekalert |