Link Between Chronic Inflammation And Cancer Confirmed
Article Date: 09 Jun 2008 - 0:00 PDT
According to scientists at the Massachussets Institute of Technology, chronic
inflammation of the intestine or stomach has been linked to DNA damage and thus
increased cancer risk. These results were released on June 2, 2008 in the
Journal of Clinical Investigation (JCI).
Inflammation can be caused by many factors, including infectious agents such as
Helicobacter pylori and Hepatitis C, which are already known to increase
cancer risk in the stomach and liver, respectively. The inflammatory response
produces cytokines, the chemicals in the immune response that encourage cell
proliferation and suppress apoptosis, which can also contribute to an increased
risk of cancer. In most normal situations, damage induced to DNA during an
inflammatory response is repaired by the cell's internal error correction system
-- but if this is not functioning properly, there is a higher chance that
mutation will occur, increasing the risk of cancer. Knowing the connection
between these factors and cancer can help doctors better guide patients who
might be at risk for inflammation induced cancers. "That variation could
influence the susceptibility of individuals and how they are going to respond to
a chronic inflammation response," said senior author Leona Samson, director of
By performing two separate studies, the team discovered that chronic
inflammation in mice generally increased the development of tumors. This was
tested additionally using mice who were already less able to repair DNA damage
and thus more susceptible to cancerous mutations. While this was long
hypothesized, these studies help confirm the idea that inflammation can be
linked to cancer. "It's something that was expected but it was never formally
proven," said lead author Lisiane Meira, research scientist in MIT's Center for
Environmental Health Sciences (CEHS).
In the JCI study, colon inflammation was induced using a chemical compound that
mimics a human colitis. This induced a higher rate of cancer. According to Meira:
"Lo and behold, the DNA repair deficient mice were more susceptible."
A second study, in collaboration with James Fox, director of the Division of
Comparative Medicine at MIT, and one of his students, Chung-Wei Lee, meant to
solidify the first. In this, mice were infected with H. pylori, and those
lacking the proper DNA repair mechanisms were more likely to have pre-cancerous
regions in the stomach. The latter study is further related to another piece
published by Fox, which showed that treating infection with this bacterium
quicly could prevent cancer development.
These results indicate that individuals who are less able to perform DNA damage
with chronic inflammation, such as ulcerative colitis, are more susceptible to
cancer than others, according to Meira. However, there is another effect of
inflamation that they postulate might influence this -- during the inflammatory
response to infection, immune cells like macrophages and neutrophils excrete
oxygen and nitrogen species that might damage DNA.
DNA damage induced by chronic inflammation contributes to colon
carcinogenesis in mice
Lisiane B. Meira, James M. Bugni, Stephanie L. Green, Chung-Wei Lee, Bo Pang,
Diana Borenshtein, Barry H. Rickman, Arlin B. Rogers, Catherine A. Moroski-Erkul,
Jose L. McFaline, David B. Schauer, Peter C. Dedon, James G. Fox and Leona D.
J. Clin. Invest. doi:10.1172/JCI35073.
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Written by Anna Sophia McKenney
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