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Vanderbilt
University researchers report they have identified a type of DNA
damage caused by chronic inflammation that may be a risk factor
for colorectal cancer.
The findings,
published in the early online edition of the Proceedings of the
National Academy of Science, suggest that measurement of this
type of DNA damage might be useful in assessment and management
of a patient's colorectal cancer risk.
"A number
of studies have implicated chronic inflammation in the development
of cancers, but the specific way that occurs is not clear,"
said Dr. Lawrence J. Marnett. "These studies suggest a direct
link between oxidative stress, like that seen in chronic inflammation,
and genetic mutations that cause human disease."
The new study
builds on years of research at Vanderbilt into how overproduction
of the inflammation-causing enzyme cyclooxygenase-2 (COX-2) may
contribute to cancer and conversely, how aspirin-like drugs
that block COX-2 might help treat or prevent cancer.
The researchers
examined a type of DNA damage caused by malondialdehye (MDA),
a product of COX-2. They found that he DNA damage had resulted
in a specific type of mutations that are common in an inherited
form of colon cancer, Hereditary Non-Polyposis Colon Cancer (HPNCC).
This work
suggests that these mutations, caused by inflammation and other
oxidative stress, might also contribute to colorectal cancer,
the researchers added.
Other
sources:
Vanderbilt University
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