UCLA cancer researchers first to link intestinal inflammation with systemic chromos...( UCLA scientists have linked for the...),Health

UCLA scientists have linked for the first time intestinal inflammation with systemic chromosome damage in mice, a finding that may lead to the early identification and treatment of human inflammatory disorders, some of which increase risk for several types of cancer.

Researchers found that local intestinal inflammation induced DNA damage to lymphocytes of the peripheral blood circulating throughout the body. This means that chromosome damage was not limited to the intestine, but involved tissues of the body distant from the site of inflammation. The team found single- and double-strand DNA breaks in the blood, and chromosome damage in peripheral blood indicating systemic genetic damage.

Inflammatory diseases have been linked to some lymphomas and abdominal, liver and colorectal cancers, said Robert Schiestl, a professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist. If inflammation can be found early before any symptoms arise - and the diseases treated immediately, it may prevent the damage that eventually leads to these cancers, he said.

The study appears in the June 1, 2009, edition of CANCER RESEARCH, the peer- reviewed journal for the American Association for Cancer Research.

"This was not known before, that intestinal inflammation causes damage that can be found throughout the body," said Schiestl, the study's senior author. "This may help explain how inflammation leads to these cancers."

Conditions that cause intestinal inflammation include Crohn's disease, inflammatory bowel disease, ulcerative colitis and Celiac disease. About 1.4 million people in the United States and 2.2 million Europeans currently suffer from inflammatory bowel diseases and incidence worldwide is increasing, Schiestl said.

The chromosome damage in the peripheral circulating blood could be used as a biomarker to identify those with intestinal inflammation be
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