How Chronic Inflammation Can Cause Cancer

Biological Engineers from the Massachusetts Institute of Technology or the MIT have discovered that the immune system can create cancerous DNA mutations when fighting off infections.

Inflammation is the last line of innate responsive defense that our body has against invading pathogens or harmful irritants. Inflammations are divided as acute and chronic.

According to the definition given by the College of Medicine of the University of Illinois, acute inflammations only occur for short durations and will only last for a minute or a few days max. This kind of inflammation usually occur with protein exudate, and is neutrophils predominate. Chronic inflammation on the other hand, can last for days or even years, mainly lymphocytic and macrophage infiltrate, and has fewer neutrophils.

According to the Cancer Network, chronic inflammation may be a causative factor in a variety of cancers. In general, the longer the inflammation persists, the higher the risk of cancer. Thus, acute inflammation, such as those that occur in response to a transient infection, is not regarded as a risk factor for the development of neoplasia, although many of the same molecular mediators are generated in both acute and chronic inflammation.

In general, inflammatory leukocytes such as neutrophils, monocytes, macrophages, and eosinophils provide the soluble factors that are thought to mediate the development of inflammation-associated cancer, although other cells, including the cancer cells themselves, also participate. This is according to a study by Emily Shacter, PhD, and Sigmund A. Weitzman, MD, both from the Cancer Network.

Chronic inflammation is a significant risk factor for cancer and other human diseases. This is stated in another study by Bogdan I. Fedelesa, Bret D. Freudenthald, Emily Yaub, Vipender Singha, Shiou-chi Changb, Deyu Lia, James C. Delaneya, Samuel H. Wilsond , and John M. Essigmann.

During chronic inflammation, cells exposed to neutrophil-derived hypochlorous acid accumulate in their genomes the DNA lesion 5-chlorocytosine (5ClC). Using a battery of chemical, structural, and genetic tools, the present study demonstrates that 5ClC is a mutagenic lesion, suggesting that genomic 5ClC accumulation could have very serious biological consequences.

5ClC induces C→T transitions, a type of mutation commonly observed in tissues under inflammatory stress as well as in the genomes of inflammation-driven cancers. Thus, the mutagenic properties of 5ClC represent an appealing molecular mechanism by which chronic inflammation induces the genetic changes that potentially enable and stimulate carcinogenesis, or the development of cancer diseases.

The complete study is published in the Proceedings of the National Academy of Sciences.

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