Inflammation and Cancer—Basic Facts

Monday, 02/07/2012  |   Inflammation, Others  |  no comments

Chronic inflammation increases cancer risk.
Subclinical, often undetectable inflammation may be as important in increasing cancer risk (for instance, obesity-induced inflammation).
Various types of immune and inflammatory cells are frequently present within tumors.
Immune cells affect malignant cells through production of cytokines, chemokines, growth factors, prostaglandins, and reactive oxygen and nitrogen species.
Inflammation impacts every single step of tumorigenesis, from initiation through tumor promotion, all the way to metastatic progression.
In developing tumors antitumorigenic and protumorigenic immune and inflammatory mechanisms coexist, but if the tumor is not rejected, the protumorigenic effect dominates.
Signaling pathways that mediate the protumorigenic effects of inflammation are often subject to a feed-forward loop (for example, activation of NF-κB in immune cells induces production of cytokines that activate NF-κB in cancer cells to induce chemokines that attract more inflammatory cells into the tumor).
Certain immune and inflammatory components may be dispensable during one stage of tumorigenesis but absolutely critical in another stage.

Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis. Inflammation also affects immune surveillance and responses to therapy. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. This review outlines the principal mechanisms that govern the effects of inflammation and immunity on tumor development and discusses attractive new targets for cancer therapy and prevention.

Inflammation can affect every aspect of tumor development and progression as well as the response to therapy. In the past ten years, we have learned a great deal about the different mechanisms by which cancer and inflammation intersect, and the time is right to translate much of the basic knowledge gained thus far and use it to add new armaments to the arsenal of cancer therapeutics. Only by targeting every single aspect of cancer biology can we expect to make real gains in the fight against these currently incurable diseases. In addition to a combination of anti-inflammatory approaches that target the tumor microenvironment with more sophisticated and selective tumoricidal drugs, future therapies should also take notice of the natural genetic variation that affects inflammation and immunity. Such considerations are extremely important in the design of new preventive approaches to the reduction of cancer risk that need to be applied to large populations composed of relatively healthy individuals. Indeed, one of the major lessons learned from investigating the relationships between inflammation and cancer is that most cancers are preventable. Prevention is a much better and more economical way to fight cancer than treating an already advanced and often intractable disease, as is done at the present.

Grivennikov SI, Greten FR, Karin M. Immunity, Inflammation, and Cancer. Cell. Volume 140, Issue 6, 19 March 2010, Pages 883–899,

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