title: Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction.
abstract: Esophageal adenocarcinoma develops in response to severe gastroesophageal reflux disease through the precursor lesion Barrett esophagus, in which the normal squamous epithelium is replaced by a columnar lining. The incidence of esophageal adenocarcinoma in the United States has increased by over 600% in the past 40 years and the overall survival rate remains less than 20% in the community. This review highlights some of the signaling pathways for which there is some evidence of a role in the development of esophageal adenocarcinoma. An increasingly detailed understanding of the biology of this cancer has emerged recently, revealing that in addition to the well-recognized alterations in single genes such as p53, p16, APC, and telomerase, there are interactions between the components of the reflux fluid, the homeobox gene Cdx2, and the Wnt, Notch, and Hedgehog signaling pathways.
authors.affiliation: Surgical Oncology Research Laboratory; Peter MacCallum Cancer Centre; East Melbourne, Australia; Sir Peter MacCallum Department of Oncology; University of Melbourne, Melbourne, Australia; Department of Surgery (St. Vincent's Hospital); University of Melbourne; Melbourne, Australia.
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Clemons
authors.affiliation: Surgical Oncology Research Laboratory; Peter MacCallum Cancer Centre; East Melbourne, Australia; Sir Peter MacCallum Department of Oncology; University of Melbourne, Melbourne, Australia; Department of Surgery (St. Vincent's Hospital); University of Melbourne; Melbourne, Australia.
authors.forename: Wayne A
authors.initials: WA
authors.lastname: Phillips
authors.affiliation: St. Vincent's Centre for Applied Medical Research; Sydney, Australia; Notre Dame University School of Medicine; Sydney, Australia.
authors.forename: Reginald V
authors.initials: RV
authors.lastname: Lord
mesh_terms: D000230:Adenocarcinoma / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D017209:Apoptosis; D001471:Barrett Esophagus / Q000150:complications / Q000473:pathology; D063646:Carcinogenesis / Q000378:metabolism / Q000473:pathology*; D018797:Cell Cycle Proteins / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D004938:Esophageal Neoplasms / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D004943:Esophagogastric Junction / Q000473:pathology*; D005764:Gastroesophageal Reflux / Q000150:complications / Q000473:pathology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D036341:Intercellular Signaling Peptides and Proteins
keywords: Barrett esophagus; adiponectin; esophageal adenocarcinoma; leptin; receptor tyrosine kinases; signaling pathways