Secondary bile acids: An underrecognized cause of colon cancer
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BioMed Central Ltd.
Abstract
Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake.A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer. © 2014 Ajouz et al.; licensee BioMed Central Ltd.
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Keywords
Bile acids and salts, Colonic neoplasms, Gastrointestinal neoplasms, Humans, Prognosis, Reactive nitrogen species, Reactive oxygen species, Bile acid, Deoxycholic acid, Dna, Epidermal growth factor receptor, Hla antigen class 1, Immunoglobulin enhancer binding protein, K ras protein, Lithocholic acid, Messenger rna, Mitogen activated protein kinase, Pregnane x receptor, Protein bcl xl, Protein kinase c, Reactive oxygen metabolite, Saturated fatty acid, Secondary bile acid, Unclassified drug, Vitamin d receptor, Aneuploidy, Apoptosis, Beef, Bile secretion, Cancer risk, Catabolism, Cell membrane, Cell proliferation, Colon cancer, Colon carcinogenesis, Colon carcinoma, Colon mucosa, Colorectal adenoma, Colorectal carcinoma, Disease association, Dna damage, Gene mutation, Genomic instability, Genotoxicity, Human, Intestine epithelium, Lipid diet, Micronucleus, Mitochondrial membrane, Oxidative stress, Positive feedback, Red meat, Review, Signal transduction, Vitamin d deficiency, Colon tumor, Complication, Metabolism, Pathophysiology