Inflammation and colorectal cancer.
Patients with long-standing inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer (CRC). However, the underlying mechanisms are not entirely clear. A genetic basis for the increased risk of CRC in IBD patients is only a partial explanation. It is possible that high levels of inflammatory mediators that are produced in this setting may contribute to the development and progression of CRC. Growing evidence supports a role for various cytokines, released by epithelial and immune cells, in the pathogenesis of IBD-associated neoplasia. Two key genes in the inflammatory process, cyclooxygenase-2 (COX-2) and nuclear factor kappaB (NF-kappaB), provide a mechanistic link between inflammation and cancer while other factors such as, TNF-alpha and IL-6-induced signaling have been recently shown to promote tumor growth in experimental models of colitis-associated cancer. This article reviews the pathogenesis of IBD-related CRC and summarizes the molecular mechanisms underlying the development of intestinal neoplasia in the setting of chronic inflammation.
Kraus
Sarah
S
Integrated Cancer Prevention Center, Tel Aviv Souraski Medical Center, 6 Weizmann Street, Tel Aviv 64239, Israel.
Arber
Nadir
N
D000818:Animals; D003092:Colitis / Q000150:complications / Q000276:immunology / Q000473:pathology; D015179:Colorectal Neoplasms / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000276:immunology / Q000473:pathology*; D018836:Inflammation Mediators / Q000502:physiology* / Q000627:therapeutic use; D015212:Inflammatory Bowel Diseases / Q000150:complications / Q000276:immunology / Q000473:pathology; D018384:Oxidative Stress / Q000276:immunology
D018836:Inflammation Mediators