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Abstract
Chronic inflammation takes part in the pathogenesis of some malignancies of the gastrointestinal tract including colorectal (CRC), gastric, and esophageal cancers. The use of ω3 polyunsaturated fatty acid (ω3-PUFA) supplements for chemoprevention or adjuvant therapy of gastrointestinal cancers is being investigated in recent years. Most evidence has been reported in CRC, although their protective role has also been reported for Helicobacter pylori-induced gastric cancer or Barrett’s esophagus-derived adenocarcinoma. Studies based on ω3-PUFA supplementation in animal models of familial adenomatous polyposis (FAP) and CRC revealed positive effects on cancer prevention, reducing the number and size of tumors, down-regulating arachidonic acid-derived eicosanoids, upregulating anti-oxidant enzymes, and reducing lipid peroxidation, whereas contradictory results have been found in induced colitis and colitis-associated cancer. Beneficial effects have also been found in FAP and ulcerative colitis patients. Of special interest is their positive effect as adjuvants on radio- and chemo-sensitivity, specificity, and prevention of treatment complications. Some controversial results obtained in CRC might be justified by different dietary sources, extraction and preparation procedures of ω3-PUFAs, difficulties on filling out food questionnaires, daily dose and type of PUFAs, adenoma subtype, location of CRC, sex differences, and genetic factors. Studies using animal models of inflammatory bowel disease have confirmed that exogenous administration of active metabolites derived from PUFAs called pro-resolving mediators like lipoxin A4, arachidonic acid-derived, resolvins derived from eicosapentaenoic (EPA), docosahexaenoic (DHA), and docosapentaenoic (DPA) acids as well as maresin 1 and protectins DHA- and DPA-derived improve disease and inflammatory outcomes without causing immunosuppression or other side effects.
Highlights
Colorectal, gastric, and esophageal cancers are among the most commonly diagnosed cancers worldwide, as well as the more frequent causes of cancer death
Other factors contributing to chronic inflammation are bacterial infections, such as Helicobacter pylori (H. pylori) infection related to gastric cancer, or non-infectious causes of inflammation, such as esophageal reflux, the main driver of Barrett’s esophagus and esophageal adenocarcinoma
During the inflammation onset phase, endogenous lipid mediators (LMs) like prostaglandins (PGs) and leukotrienes (LTs) are released from arachidonic acid (AA) acting as go signals for inflammation, increasing vascular permeability that enables polymorphonuclear leukocyte (PMN) infiltration into the damaged tissue, and afterwards, prostaglandins (PGE2 and PGD2) acting as stop signals mark the end of acute inflammation and the beginning of LM-class switching process by transcriptional activation of 15-lipoxygenase (15-LOX) in neutrophils and producing the first class of endogenous specialized pro-resolving lipid mediator (SPM), AA-derived, called lipoxins (LXs), stop-and-go signals for inflammation and resolution phases (Qiu et al, 2001; Nathan, 2002; Serhan, 2007)
Summary
Colorectal, gastric, and esophageal cancers are among the most commonly diagnosed cancers worldwide, as well as the more frequent causes of cancer death.
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