Cellular origins and molecular mechanisms of Barrett's esophagus and esophageal adenocarcinoma.

Abstract

This paper presents commentaries on animal models used for Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) research; acid- and bile-induced chromosomal instability and clonal selection during the progression of BE to EAC; how the components of gastric refluxate, especially acid and bile salts, promote carcinogenesis in metaplastic BE; genome-wide changes in DNA methylation and transcription involved in BE carcinogenesis; the potential role of miRNA in the development of BE and EAC; the effect of inflammatory cytokines linked to obesity on the activation of cell-death pathways and cell survival in BE and esophageal cancer; and the role of autophagy in esophageal cancer development.

• Authors: Yu Fang, Xiaoxin Chen, Manisha Bajpai, Amit Verma, Kiron M Das, Rhonda F Souza, Katherine S Garman, Claire L Donohoe, Naoimh J O'Farrell, John V Reynolds, Katerina Dvorak
• Journal: Annals of the New York Academy of Sciences (Ann N Y Acad Sci) Vol. 1300 Pg. 187-199 (Oct 2013) ISSN: 1749-6632 [Electronic] United States
• PMID: 24117642 (Publication Type: Journal Article, Review)
• Copyright: © 2013 New York Academy of Sciences.

Chemical References

• Biomarkers, Tumor

Topics

• Adenocarcinoma (genetics, metabolism, pathology)
• Animals
• Barrett Esophagus (genetics, metabolism, pathology)
• Biomarkers, Tumor (genetics, metabolism)
• Cell Transformation, Neoplastic (genetics, metabolism, pathology)
• DNA Methylation
• Disease Models, Animal
• Esophageal Neoplasms (genetics, metabolism, pathology)
• Humans