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Blocking COX-1 slows tumor growth in mice

an tumors. Most of these, however, used antibodies to detect COX-2 expression. "We now know that many of the commercially available antibodies cross react with both COX-1 and COX-2," Dey said.

The Vanderbilt researchers used multiple techniques, and in 2003 reported that COX-1 was over-expressed and promoted the growth of blood vessels in human epithelial ovarian tumors.

A year earlier, Sandra Orsulic, Ph.D., and her colleagues at the Memorial Sloan-Kettering Cancer Center in New York reported that they were able to induce ovarian cancer in a mouse model by using a virus to deliver two cancer-causing genes into ovarian surface epithelial cells that lacked a tumor suppressor gene.

In the current study, the Vanderbilt researchers used Orsulic's model to test whether celecoxib (Celebrex), a selective COX-2 inhibitor, and SC-560, an experimental drug that selectively blocks COX-1, slowed tumor growth when these cells were transplanted into mice.

They found that while Celebrex had little effect, the COX-1 blocker dramatically reduced tumor growth. The drug also blocked production by COX-1 of prostacyclin, a member of a family of potent, hormone-like substances called prostaglandins that play a role in a wide variety of physiological functions including pain, inflammation and, presumably, cancer.

Whereas prostacyclin is the predominant prostaglandin found in mouse ovarian tumors, another prostaglandin, PGE2, seems to be generated in higher quantities in human ovarian cancers. This suggests that it's not the particular enzyme COX-1 or COX-2 but downstream factors, including prostaglandins, that initiate tumor growth, Dey said.

Last fall, for example, the Vanderbilt researchers reported that silencing a cellular receptor called PPAR interfered with the ability of PGE2 to promote pre-cancerous colon polyps in mice.

Other researchers who contributed to the ovarian cancer study were Dingzhi Wang, Ph.D., research associate professor of
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Contact: Clinton Colmenares
clinton.colmenares@vanderbilt.edu
615-322-4747
Vanderbilt University Medical Center
1-May-2005


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