June 27, 2013
One of the most promising cancer prevention targets to emerge in the 1990s was the enzyme cyclooxygenase-2 (COX-2). Raymond Dubois, M.D., Ph.D., and his lab were the first in the world to report that COX-2 expression is elevated in human colorectal cancers and that inhibitors of the enzyme block the growth of colorectal cancer cells that express COX-2.
This corroborated the epidemiological observation that people who take non-steroidal anti-inflammatory drugs (NSAIDs) on a regular basis have a reduced incidence of colorectal cancer. One of the known effects of these aspirin-like drugs is their ability to inhibit COX-2.
COX-2 is an enzyme normally expressed at sites of inflammation and is suspected to play a role in the control of cell growth. DuBois’ research demonstrated that COX-2 is highly expressed in 85-90 percent of human colon cancers and 45 percent of benign tumors, but is undetectable in normal colon tissue.
A flurry of development and study of aspirin-like COX-2 inhibitors (like Celebrex and Vioxx) followed, but excitement cooled when long-term use of these drugs showed increased risk for heart attack and stroke.
Larry Marnett, Ph.D., and the A.B. Hancock Jr. Memorial Laboratory are now developing a series of imaging agents targeted to COX-2. The agents have fluorescent tracers that make it possible to see tumors in their earliest stages by detecting increasing levels of COX-2. It may even be possible to use the imaging agents to deliver cancer-killing medicines directly to tumor cells that express COX-2.
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