Bile acids as endogenous etiologic agents in gastrointestinal cancer - PubMed (original) (raw)

Editorial

Bile acids as endogenous etiologic agents in gastrointestinal cancer

Harris Bernstein et al. World J Gastroenterol. 2009.

Abstract

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.

PubMed Disclaimer

Figures

Figure 1

Figure 1

The role of bile acids in the sequence of events leading to gastrointestinal cancer.

References

    1. Bernstein H, Bernstein C, Payne CM, Dvorakova K, Garewal H. Bile acids as carcinogens in human gastrointestinal cancers. Mutat Res. 2005;589:47–65. - PubMed
    1. Reddy BS. Diet and excretion of bile acids. Cancer Res. 1981;41:3766–3768. - PubMed
    1. Cherbonnel-Lasserre C, Gauny S, Kronenberg A. Suppression of apoptosis by Bcl-2 or Bcl-xL promotes susceptibility to mutagenesis. Oncogene. 1996;13:1489–1497. - PubMed
    1. Cherbonnel-Lasserre C, Dosanjh MK. Suppression of apoptosis by overexpression of Bcl-2 or Bcl-xL promotes survival and mutagenesis after oxidative damage. Biochimie. 1997;79:613–617. - PubMed
    1. Saintigny Y, Dumay A, Lambert S, Lopez BS. A novel role for the Bcl-2 protein family: specific suppression of the RAD51 recombination pathway. EMBO J. 2001;20:2596–2607. - PMC - PubMed

Publication types

MeSH terms

Substances

Grants and funding

LinkOut - more resources