Machines Like Us

As in the previous prostate cancer study, which was also conducted by USC researchers and published in the April 2007 edition of Nature Genetics, the colorectal cancer risk factor is located in a region of the human genome devoid of known genes on chromosome 8. The study’s complete findings will be published in the July 8 online edition of Nature Genetics.

“This is an important finding because, for the first time, a common genetic risk factor for multiple cancers has been identified,” says lead author Christopher Haiman, assistant professor of preventive medicine at the Keck School of Medicine of USC. Adding, “There appears to be something fundamental occurring in this region that influences not only colorectal and prostate cancer, but perhaps cancers in general.” (Another recently published study, in which USC researchers also were involved, identified variants in this same chromosomal region as playing a predictive role relative to the risk of developing breast cancer.)

For the current colorectal cancer study, the USC team genotyped six of the seven variants previously identified as increasing the risk of prostate cancer development. The samples analyzed totaled 1,807 invasive colorectal cancer cases and 5,511 controls. These samples were drawn from five populations (African Americans, Japanese Americans, Native Hawaiians, Latinos, and European Americans) included in the Multiethnic Cohort Study, an epidemiological study of more than 215,000 people from Los Angeles and Hawaii created in 1993 by Brian Henderson, dean, Keck School of Medicine of USC, and Laurence Kolonel of the University of Hawaii.

According to Henderson, co-author of the colorectal cancer study, “Having previously identified several genetic risk factors related to prostate cancer, and now having identified one of these same variants as predictive of colorectal cancer risk, brings us closer to our long-term goal of developing a model that more precisely pinpoints who is at greater risk for developing colorectal, prostate, and other cancers.” However, Henderson notes, “We still need to identify the biological mechanism through which these variants are influencing the development of various cancers.”

University of Southern California