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.
Original language | English (US) |
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Pages (from-to) | 187-199 |
Number of pages | 13 |
Journal | Annals of the New York Academy of Sciences |
Volume | 1300 |
Issue number | 1 |
DOIs | |
State | Published - Oct 2013 |
All Science Journal Classification (ASJC) codes
- General Neuroscience
- General Biochemistry, Genetics and Molecular Biology
- History and Philosophy of Science
Keywords
- Autophagy
- Barrett's esophagus
- DNA methylation
- Esophageal adenocarcinoma
- Obesity