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Rresearchers
at Dana-Farber Cancer Institute report they have identified a
mechanism by which non-steroidal anti-inflammatory drugs (NSAIDs)
inhibit the development of colon cancer.
Compared with
normal cells, colorectal cancer cells have abnormally high levels
of an immune system protein, IL-6. The IL-6 protein triggers malignant
growth by activating a protein called STAT1, which transmits signals
that prevent the normal scheduled death of cells in the colon.
Dr. David
Frank said in laboratory tests in which colon cancer cells were
treated with NSAIDs such as ibuprofen, aspirin and sulindac, they
blocked the IL-6 activation of STAT1, throwing a wrench into the
signaling pathway leading to cancer.
The researchers
said they also applied butyrate, a chemical that's produced when
the body metabolizes dietary fiber, and it also blocked IL-6 activity,
but through a different signaling pathway.
Frank said
he and his colleagues are now tudying ways to block the STAT1
protein in patients who have already developed colorectal cancers.
The findings
are published in the Proceedings for the 2003 Annual Meeting of
the American Association for Cancer Research.
Other
Sources: American Association for Cancer Research
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