Open AccessBile acids as endogenous etiologic agents in gastrointestinal cancer
Author(s) -
Harris Bernstein,
Carol Bernstein,
Claire M. Payne,
Katerina Dvorak
Publication year - 2009
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.15.3329
Subject(s) - cancer , colorectal cancer , carcinogenesis , biology , gastrointestinal tract , gastrointestinal cancer , bile acid , pancreatic cancer , rectum , dna damage , carcinogen , pancreas , deoxycholic acid , medicine , esophagus , stomach , gastroenterology , cancer research , endocrinology , dna , biochemistry
Bile acids are implicated as etiologic agents in cancer of the gastrointestinal (GI) tract, including cancer of the esophagus, stomach, small intestine, liver, biliary tract, pancreas and colon/rectum. Deleterious effects of bile acid exposure, likely related to carcinogenesis, include: induction of reactive oxygen and reactive nitrogen species; induction of DNA damage; stimulation of mutation; induction of apoptosis in the short term, and selection for apoptosis resistance in the long term. These deleterious effects have, so far, been reported most consistently in relation to esophageal and colorectal cancer, but also to some extent in relation to cancer of other organs. In addition, evidence is reviewed for an association of increased bile acid exposure with cancer risk in human populations, in specific human genetic conditions, and in animal experiments. A model for the role of bile acids in GI carcinogenesis is presented from a Darwinian perspective that offers an explanation for how the observed effects of bile acids on cells contribute to cancer development.