A new view of cancer  pg. 2

For nearly a century and a half, scientists have suspected that many cancers are caused by inflammation—the complicated process by which the body heals wounds and fights off invading pathogens.

Prime examples: colorectal cancer in patients with inflammatory bowel disease; lung cancer that follows chronic inflammation from inhaled asbestos particles; and tumors of the stomach and liver—among the most common cancers worldwide—that are linked to pathogen-induced inflammation. Inflammation also may contribute to the development of prostate cancer, which, next to lung cancer is the second leading cancer killer in American men.

Another link in this causal chain was forged about 10 years ago, when population-based studies detected a 40 percent to 50 percent drop in the relative risk of developing colorectal cancer among people who regularly use aspirin.

The finding came at a fortuitous moment: during the previous two decades, scientists had learned that aspirin worked by blocking production of prostaglandins, ubiquitous lipid-signaling molecules that are involved in a host of physiological processes. Two prostaglandin-generating enzymes, the cyclooxygenases, had been identified, and one of them—COX-2—was known to play an important role in pain and inflammation.

In 1994, Raymond N. DuBois, M.D., Ph.D., and his colleagues at Vanderbilt University Medical Center found high levels of COX-2 in cancerous colon tissue. Three years later, they had stopped human colon cancer cells from growing in the laboratory by blocking the COX-2 enzyme.

By this time, Celebrex—the first selective COX-2 inhibitor—was on its way to market for treatment of rheumatoid arthritis. Researchers began testing the drug in patients with familial adenomatous polyposis (FAP), an inherited condition characterized by the appearance of multiple polyps in the colon that nearly always become malignant. In June 2000, an international team of researchers, including DuBois and Hawk, reported that the use of Celebrex led to a significant reduction in the number of polyps in patients with FAP.

The landmark finding, published in The New England Journal of Medicine, opened the floodgates for studies aimed at preventing other cancers by blocking production of prostaglandins. Since then, DuBois and his colleagues have found that one of the members of the prostaglandin family, PGE2, seems to be specifically involved in spurring the proliferation and invasive potential of colorectal cancer cells, and it may do so—at least in part—through the receptor for epidermal growth factor (EGF), which stimulates cell growth.

“This is what I’m really excited about,” says DuBois, since 2007 provost and executive vice president for academic affairs at the University of Texas M. D. Anderson Cancer Center. “It just continues to support our whole concept from 1994, that (COX-2) is really playing a role” in colon cancer.

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