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Cellular origins and molecular mechanisms of Barrett's esophagus and esophageal adenocarcinoma
Author(s) -
Fang Yu,
Chen Xiaoxin,
Bajpai Manisha,
Verma Amit,
Das Kiron M.,
Souza Rhonda F.,
Garman Katherine S.,
Donohoe Claire L.,
O'Farrell Naoimh J.,
Reynolds John V.,
Dvorak Katerina
Publication year - 2013
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12249
Subject(s) - carcinogenesis , barrett's esophagus , esophagus , cancer research , dna methylation , esophageal cancer , autophagy , esophageal adenocarcinoma , adenocarcinoma , biology , transcription factor , cancer , medicine , apoptosis , gene , genetics , gene expression
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.