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Prostate Cancer Gene Also Raises Colon Cancer Risk
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Page: << Prev | 1 | 2 | 3 | Next >> The California team stressed that the level of risk to an individual conferred by the gene did not change, regardless of the person's sex, race, site of tumor, tumor stage or the presence of colon cancer risk factors such as family history, smoking or drinking.
However, rs6983267 was found more frequently in some ethnicities than in others. "The frequency of this specific genetic variation varies widely in the population -- from about 85 percent of African-Americans to as low as 30 percent of Japanese," Haiman said.
Carrying rs6983267 does not place any individual black American at an extraordinarily higher risk for colon cancer, Haiman explained. However, due to its relative high prevalence among blacks, it probably accounts for about 40 percent of all cases of colorectal cancers among this minority, he said.
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Another researcher noted that genes like the one in region 8q24 are often more dangerous when they clump together in the same person.
"Although individually these markers may only contribute small amounts of risk, collectively, in certain individuals, they may actually have composite risks which are comparable to that of known, high-risk [mutations]," explained Dr. Richard Houlston, of the Institute of Cancer Research in Sutton, U.K.
Comparing genomic differences among 930 people with colorectal cancer and 960 controls, his team also zeroed in on rs6983267 as boosting tumor risk. Given the genes' link to prostate cancer, "it does tend to suggest that some of these things may actually have a generic effect on more than one malignancy," Houlston said at the press conference.
A fourth study -- this time led by a consortium from Israel, Spain and the United States -- uncovered a similar connection between genetic variations on 8q24 and a rise in colon cancer risk. That research was published in the July issue of Cancer Biology and Therapy.
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Copyright © 2007 ScoutNews, LLC. All rights reserved.
Last updated 7/9/2007
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SOURCES: July 6, 2007, Nature Genetics news conference, with Malcolm Dunlop, M.D., researcher, Cancer Research UK, and head, Colon Cancer Genetics Group, University of Edinburgh, Scotland; Christopher Haiman, Sc.D., assistant professor, Keck School of Medicine, University of Southern California, Los Angeles; and Richard Houlston, M.D., Ph.D., professor, molecular and population genetics, Institute of Cancer Research, Sutton, U.K.; Durado Brooks, M.D., director, prostate and colorectal cancer, American Cancer Society, Atlanta; July 8, 2007, Nature Genetics; July 2007, Cancer Biology and Therapy
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