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Pregnancy Timeline by SemestersFemale Reproductive SystemFertilizationThe Appearance of SomitesFirst TrimesterSecond TrimesterThird TrimesterFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterDevelopmental Timeline
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June 13, 2012--------News Archive Return to: News Alerts


Endoscopic biopsy shows granulomatous inflammation of the colon in Crohn's disease.

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How Inflammation Can Lead to Cancer

New study gives comprehensive look at how changes that occur due to inflammation can progress to cancer

One of the biggest risk factors for liver, colon or stomach cancer is chronic inflammation of those organs, often caused by viral or bacterial infections. A new study from MIT offers the most comprehensive look yet at how such infections provoke tissues into becoming cancerous.

The study, which is appearing in the online edition of Proceedings of the National Academy of Sciences the week of June 11, tracked a variety of genetic and chemical changes in the livers and colons of mice infected with Helicobacter hepaticus, a bacteria similar to Helicobacter pylori, which causes stomach ulcers and cancer in humans.

The findings could help researchers develop ways to predict the health consequences of chronic inflammation, and design drugs to halt such inflammation.

“If you understand the mechanism, then you can design interventions,” says Peter Dedon, an MIT professor of biological engineering. “For example, what if we develop ways to block or interrupt the toxic effects of the chronic inflammation?”

For the past 30 years, Tannenbaum has led a group of MIT researchers dedicated to studying the link between chronic inflammation and cancer. Inflammation is the body’s normal reaction to any kind of infection or occassional damage. But, when inflammation goes on for too long, tissues can remain damaged and not recover.

When the body’s immune system detects pathogens or cell damage, it activates an influx of cells called macrophages and neutrophils. These cells engulf bacteria, dead cells and debris, as well as proteins, nucleic acids and other molecules released by dead or damaged cells. As part of this clean-up process, immune cells produce highly reactive chemicals that help degrade the bacteria.

“In doing this, in engulfing the bacteria and dumping these reactive chemicals on them, the chemicals also diffuse out into the tissue, and that’s where the problem comes in,” Dedon says.

If sustained over a long period, inflammation can eventually lead to cancer. A recent study published in the journal The Lancet found that infections account for about 16 percent of new cancer cases worldwide.

In the new MIT study, researchers analyzed mice infected with H. hepaticus, causing them to develop inflammatory bowel disease similar to what is found in humans. Over the course of 20 weeks, the mice developed chronic infections of the liver and colon, with some cases advancing to colon cancer.

Throughout the 20-week period, the researchers measured about a dozen different types of damage to DNA, RNA and proteins. They also examined tissue damage and measured which genes were turned on and off as the infection progressed. One of their key findings was that the liver and colon responded differently to infection.

In the colon, but not the liver, neutrophils secreted hypochlorous acid (also found in household bleach), which significantly damages proteins, by adding a chlorine atom to DNA and RNA. The hypochlorous acid is meant to kill bacteria, but it also leaks into surrounding tissue and damages the epithelial cells of the colon.

Researchers found levels of one of the chlorine-damage products - chlorocytosine - in DNA and RNA, which correlated well with the severity of the inflammation. Finding this relationship could lead to an ability to predict the risk for cancer developing in chronic inflammation patients with infections of the colon, liver or stomach.

Tannenbaum recently identified another chlorine-damaging product in proteins: chlorotyrosine, which also correlates with inflammation. While both of these observations point to an important role for neutrophils in inflammation and cancer, “we don’t know yet if we can predict the risk for cancer from these damaged molecules,” Dedon says.

Another difference the researchers found between the colon and the liver was that DNA repair systems became more active in the liver but less active in the colon, even though both were experiencing DNA damage. “It’s possible that we have kind of a double whammy [in the colon]. You have this bacterium that suppresses DNA repair, at the same time that you have all this DNA damage happening in the tissue as a result of the immune response to the bacterium,” Dedon says.

The researchers also identified several previously unknown types of damage to DNA in mice and humans, one of which involves oxidation of guanine, a building block of DNA, with two new products, spiroiminodihydantoin and guanidinohydanotoin.

James Swenberg, a professor of environmental sciences and engineering at the University of North Carolina School of Public Health, says the “comprehensive and innovative” study should help researchers better understand many types of cancer. “I can’t remember ever seeing a paper that brought so many aspects of research to the table in one report,” says Swenberg, who was not involved in the study.

In future studies, the MIT team plans to investigate the mechanisms of cancer development in more detail, including looking at why cells experience an increase in some types of DNA damage but not others.

The research was funded by the National Cancer Institute.

Peter Dedon is one of four senior authors of the paper, along with Steven Tannenbaum, a professor of biological engineering and chemistry; James Fox, a professor of biological engineering and director of the Department of Comparative Medicine; and Gerald Wogan, a professor of biological engineering and chemistry. Lead author is Aswin Mangerich, a former MIT postdoc now at the University of Konstanz in Germany.

Original article: http://web.mit.edu/newsoffice/2012/cancer-inflammation-h-pylori-0611.html