The Link between Inflammation and Cancer

A research team from the Center for Environmental Health Sciences (CEHS) at MIT has confirmed that when DNA repair mechanisms are compromised, chronic inflammation expedites intestine cancer in mice. The results suggest that people with a decreased ability to repair DNA damage might be more susceptible to developing cancer associated with chronic inflammation, such as ulcerative colitis. This discovery may lead to the development of treatments for the prevention of various types of cancer and will hopefully raise the awareness to the importance of early detection and treatment of inflammation.

Inflamation Pathway (Credit:National Institute of General Medical Sciences)
Inflamation Pathway (Credit: Array Biopharma)

Inflammation caused by infectious agents, such as Helicobacter pylori and Hepatitis C, is known to increase the risk of stomach and liver cancers, respectively. It is well known that inflammation produces cytokines (immune response chemicals that encourage cell proliferation and suppress cell death), which could lead to cancer if proper cell monitoring mechanisms are not activated.

In addition, another process that is evoked during inflammation has been suspected as a possible cancer inducer. During the inflammatory response to infection, immune cells, such as macrophages and neutrophils, release reactive elements, such as oxygen and nitrogen, often damaging the DNA.

When DNA repair mechanisms function properly, the damage caused by inflammation is repaired before it can develop into cancer. However, the MIT team showed that once the mechanisms are not intact, the damage to the DNA can develop into mutations, possibly leading to cancer. The effectiveness of these processes varies between different people and there are many reasons for the deficiency of DNA repair mechanisms, including genetic mutations, aging, or a diet lacking in vitamins E, C, and folic acid. These interpersonal differences can influence the susceptibility and the nature of different individuals’ response to chronic inflammation.

In the study, a research team led by Lisiane Meira and Leona Samson tested two groups of mice: the first group was comprised of healthy mice and served as the control group, while the other group was comprised of mice with genetically impaired DNA repair mechanisms. The researchers induced colon inflammation in the mice by treating them with a chemical compound that creates a condition similar to human colitis. The results were not surprising, and showed that the mice with DNA repair deficiency were more susceptible to cancer.

 Inflammation and Cancer (Credit: National Institute of General Medical Sciences)
Inflammation and Cancer
(Credit: National Institute
of General Medical Sciences)

The team then conducted 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. This study was conducted in order to show that different types of infections could replicate the results of the first study. The outcome was as expected – when infected with H. pylori, mice lacking the proper DNA repair mechanisms were more susceptible to pre-cancerous lesions in the stomach.

This study is related to another article by Fox, which showed that treating H. pylori infection at the early stages with antibiotics can prevent cancer development. The new study suggests that if H. pylori inflammation goes untreated, patients with deficient DNA repair mechanisms would stand at a greater risk of developing cancer. This discovery will hopefully alert doctors and patients to the dangers of many types of inflammation. It is obvious that there is much to be gained from further research of the link between inflammation and cancer. 

TFOT recently covered a research project in which a trail receptor, related to the link between inflammation and cancer, was discovered by scientists at the University of Pennsylvania. Another recent breakthrough in cancer research was the creation of cancer-resistant mice by researchers from the University of Kentucky. 

The original MIT press release can be found here.