[Editors] EMBARGOED: MIT confirms link between inflammation, cancer

[Teresa Herbert]

EMBARGOED for 5 p.m. ET, Monday, June 2, 2008

Contact: Teresa Herbert, MIT News Office -- Phone: 617-258-5403 --  
Email: therbert at mit.edu

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MIT confirms link between inflammation, cancer
--Chronic stomach inflammation damages DNA, increasing cancer risk
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Chronic inflammation of the intestine or stomach can damage DNA,  
increasing the risk of cancer, MIT scientists have confirmed.

The researchers published evidence of the long-suspected link in the  
June 2 online issue of the Journal of Clinical Investigation (JCI).

In two studies, the researchers found that chronic inflammation  
accelerated tumor formation in mice lacking the ability to repair DNA  
damage.

“It’s something that was expected but it was never formally proven,”  
said Lisiane Meira, research scientist in MIT’s Center for  
Environmental Health Sciences (CEHS) and lead author of the paper.

The results of this work suggest that people with decreased ability to  
repair DNA damage might be more susceptible to developing cancer  
associated with chronic inflammation such as ulcerative colitis, Meira  
said.

Inflammation caused by infectious agents such as Helicobacter pylori  
and Hepatitis C is known to increase the risk of stomach and liver  
cancers, respectively. Researchers have long known that inflammation  
produces cytokines (immune response chemicals that encourage cell  
proliferation and suppress cell death), which can lead to cancer.

In addition, it was suspected that another effect of the inflammation  
pathway could also induce cancer. During the inflammatory response to  
infection, immune cells such as macrophages and neutrophils release  
reactive oxygen and nitrogen species that can damage DNA.

Under normal circumstances, the DNA damage induced during an  
inflammatory response is repaired by DNA repair systems. But, if the  
DNA repair system is not functioning properly, that damage can induce  
mutations that can lead to cancer, according to the new study.

Every individual has variations in the effectiveness of their DNA  
repair systems, which could help doctors figure out which patients are  
most susceptible to inflammation-induced cancers.

“That variation could influence the susceptibility of individuals and  
how they are going to respond to a chronic inflammation response,”  
said Leona Samson, senior author of the study and director of the CEHS.

In the JCI study, the researchers induced colon inflammation in the  
mice by treating them with a chemical compound that creates a  
condition similar to human colitis. “Lo and behold, the DNA repair  
deficient mice were more susceptible” to cancer, said Meira.

To show that this is a general phenomenon, the team did a second  
study, in collaboration with another CEHS member, James Fox, director  
of the Division of Comparative Medicine at MIT, and one of his  
students, Chung-Wei Lee. They showed that mice infected with H.  
pylori, who also lacked the proper DNA repair mechanisms, were more  
susceptible to pre-cancerous lesions in the stomach.

This study is related to another recent paper published by Fox, which  
found that treating H. pylori infection early with antibiotics can  
prevent cancer development. The new study suggests that if H. pylori  
goes untreated, patients with poorly functioning DNA repair mechanisms  
would have a greater risk of developing cancer.

Other CEHS faculty involved in the JCI report were Peter Dedon and  
David Schauer.  The research was funded by the National Institutes of  
Health.

By Anne Trafton, News Office


# # #


Teresa Herbert
Media Specialist
Massachusetts Institute of Technology
News Office, Room 11-400
Cambridge, MA 02139-4307

Phone: 617-258-5403
Fax: 617-258-8762

therbert at mit.edu




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