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Enzyme deficiency may contribute to liver cancer, Mount Sinai research indicates

(Toronto, Ontario, July 27, 2005) Primary liver cancer is much more likely to take root when a naturally occurring enzyme is in short supply, a team of researchers has found at Mount Sinai Hospital's Samuel Lunenfeld Research Institute.

Using a knockout mouse model, the team has found that the likelihood of hepatoma, or primary liver cancer, increases substantially when half the normal amount of an enzyme called Plk4 is present. Furthermore, 60 per cent of patients with hepatoma were missing one copy of the Plk4 gene in their cancers. The genetic basis for hepatoma has not previously been extensively explored.

The study is published today in the August edition of the prestigious science journal, Nature Genetics.

"Our study indicates that loss of one copy of Plk4 is a major risk factor for primary liver cancer," says Dr. Carol Swallow, a surgical oncologist at Mount Sinai Hospital and an Associate Professor of Surgery at University of Toronto.

"This represents a major advance in our understanding of hepatoma at a molecular level and provides insight into who may be predisposed to this type of cancer genetically."

Dr. Swallow and her co-investigators, Dr. Jim Dennis, Senior Investigator at the SLRI, and Mike Ko, a PhD candidate at the University of Toronto, believe that this finding has important implications for screening and early detection.

The American Cancer Society estimates that there will be 667,000 new cases of liver cancer worldwide in 2005, with 83 per cent of them occurring in developing countries, particularly in Southeast Asia. The disease is also more prevalent in men than it is in women.

"Unlike many common cancers, the incidence of hepatoma is increasing in both developed and developing countries," said Dr. Swallow.


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Contact: Emily Hanft
416-586-3161
University of Toronto
27-Jul-2005


Page: 1

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