Omega Balance by Anthony John Hulbert

Author:Anthony John Hulbert
Language: eng
Format: epub
Publisher: Johns Hopkins University Press
Published: 2022-06-15T00:00:00+00:00

Chronic Inflammation and Cancer

The idea that cancer and inflammation are linked is old. In 1863, Rudolf Virchow observed that macrophages were part of cancer tumors and furthermore proposed that chronic irritation and inflammation cause cancer. For many years, his theory was ignored, but in the past few decades the links between inflammation, the immune system, and cancer have become very active areas of research with exciting implications for prevention and treatment.

In the normal situation, most of our cells do not divide uncontrollably; this is mediated by a number of genes. It is the mutation of these genes that leads to uncontrolled cell division and in turn cancerous growth. While the basis of cancer involves genetic mutations, the microenvironment of the tumor is also a very important influence, and it is likely through such an effect that cancer and inflammation connect.

White blood cells are found in tumors and in some cases may account for as much as half of the total mass of the tumor.80 It has been estimated that about 25 percent of cancers are associated with chronic inflammation (see note 80). Several diseases of chronic inflammation are associated with cancer. For example, having inflammatory bowel disease can dramatically increase the risk of later colorectal cancer.81 Inflammatory cytokines are produced by both the cancer cells and inflammatory cells in tumors and have become a focus of development of some anticancer therapies.82

Macrophages are intimately involved in assisting the process of metastasis. Macrophages present in the tumor facilitate the growth of new blood vessels and the breakdown of the extracellular environment. By direct communication with the cancerous cells of the tumor, they assist the entry of cancer cells into blood vessels and their consequent spread to other parts of the body. Macrophages are obligate partners for tumor cell migration, invasion, and metastasis,83 and the fats in their cell membranes are important contributors to the production of the inflammation mediators involved in this activity.

The enzymes responsible for production of eicosanoids (from 20:4ω-6) are elevated in several types of tumor, and the prostaglandins produced enhance the spread of cancer cells (see note 82). Aspirin and other NSAIDS that inhibit these enzymes have been shown to reduce both the risk of developing cancer and the growth of a number of cancers (see note 82) Many inflammation mediators are also elevated in cancer. Paradoxically, although tumor necrosis factor (TNF) was initially named because of its antitumor activity, its serum concentration is elevated in many cancer patients, and it is associated with tumor cell growth, survival, and invasion of tumor cells as well as the growth of new blood vessels in tumors (see note 82).

An often-used marker of inflammation is the plasma concentration of C-reactive protein (CRP). The Copenhagen City Heart Study, started in 1976–78, measured plasma CRP in adults who did not have cancer. It found that 14 percent had no inflammation (less than 1mg per L), 61 percent had mild chronic inflammation (1–3mg per L), while 25 percent had moderate chronic inflammation (more than 3mg per L).

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