Molecular alterations during development of esophageal adenocarcinoma.
The incidence of esophageal adenocarcinoma has risen significantly over the last decades. During esophageal carcinogenesis many molecular alterations occur that disrupt essential cellular processes, directing the cell to a rapidly proliferating, immortal state. The chronic inflammation that is present in Barrett's esophagus creates an environment in which such molecular alterations are both induced and tolerated. Here, the novel insights in the molecular mechanisms that underlie the development of esophageal adenocarcinoma are reviewed, focusing on the role of inflammation, angiogenesis, apoptosis inhibition, loss of cell cycle control, and loss of cell-cell adhesion. These novel developments will open new perspectives for diagnosis, treatment, and prevention of esophageal adenocarcinoma.
Bax
Dorine A
DA
Department of Gastroenterology and Hepatology, Erasmus MC - University Medical Center Rotterdam, Rotterdam, The Netherlands.
Siersema
Peter D
PD
Van Vliet
Arnoud H M
AH
Kuipers
Ernst J
EJ
Kusters
Johannes G
JG
D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology*; D017209:Apoptosis; D016718:Arachidonic Acid / Q000378:metabolism; D001471:Barrett Esophagus / Q000473:pathology*; D000071616:CDX2 Transcription Factor; D002448:Cell Adhesion / Q000502:physiology; D002453:Cell Cycle; D049109:Cell Proliferation; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology*; D005753:Gastric Mucosa / Q000473:pathology; D018398:Homeodomain Proteins / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008679:Metaplasia / Q000473:pathology; D008967:Molecular Biology; D009389:Neovascularization, Pathologic / Q000378:metabolism
D000071616:CDX2 Transcription Factor; C491270:CDX2 protein, human; D018398:Homeodomain Proteins; D016718:Arachidonic Acid