Details Linking Chronic Inflammation and Cancer Continue To Emerge

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New insights into potential mechanisms behind the body’s inflammatory responses and links to cancer continue to surface. One study, from the University of California, San Diego, School of Medicine, offered new details about microbial-dependent mechanisms through which some cancers mount an inflammatory response to fuel development and growth. The findings are published in the Nov. 7, 2012, online edition of Nature .

Lead researcher Sergei Grivennikov, Ph.D., said the goal was to investigate mechanisms responsible for tumor-elicited inflammation in a mouse model of colorectal tumorigenesis. Grivennikov said the model exhibited upregulation of the cytokines interleukin 23 (IL-23) and IL-17, similar to human colorectal cancer.

The UCSD research team, which included principal investigator Michael Karin, Ph.D., distinguished professor of pharmacology and head of the Laboratory of Gene Regulation and Signal Transduction, found that developing tumors disrupt tissue homeostasis, partly because they lack a particular protective protein coating and a tight seal between their epithelial cells. “Many epithelial cancers develop proximally to these microbial communities,” said Grivennikov. “Without that coating and the cellular seal, ordinarily benign, commensal microorganisms present in the colon can enter the tumor to be recognized by immune cells as invaders, launching an inflammatory reaction.”