title: Is Barrett's esophagus the precursor of most adenocarcinomas of the esophagus and cardia? A biochemical study.
abstract: OBJECTIVE
  To obtain biochemical evidence that Barrett's esophagus (BE) is the precursor of most adenocarcinomas (Adc) of the esophagus and cardia.
  
  
  BACKGROUND
  Based on morphologic data, BE was previously proposed as the precursor of most Adc of the esophagus. This hypothesis would receive strong support if biochemical evidence were found to demonstrate a pattern common to BE and Adc of the esophagus and cardia.
  
  
  METHODS
  We studied the presence of intestinal-type proteins sucrase-isomaltase (SI) and crypt Cell Antigen (CCAg) in BE, Barrett's Adc, and esophageal-cardial Adc without BE. In each case specimens were collected from normal esophagus, stomach, tumor, and BE mucosa when present. To study related conditions, five specimens of peptic esophagitis and of squamous cell carcinoma were also analyzed. An indirect immunofluorescence technique was employed and sections were analyzed with laser confocal microscopy imaging.
  
  
  RESULTS
  Most Barrett's mucosa specimens stained positively for SI (93%) and CCAg (89%). These proteins were detected in BE independently of the type of metaplasia, the coexistence of dysplasia, or the presence of associated Adc. SI and CCAg were present in 25 (96%) and 24 (92%) of the cases of Adc respectively. No statistical difference was detected in SI and CCAg expression between Adc samples with and without BE, between BE and Adc samples with or without BE, and between tumors located in the esophagus versus the cardia. No staining for these proteins was detected in stomach or esophageal mucosa, in submucosal glands of the esophagus, in peptic esophagitis or squamous cell carcinoma.
  
  
  CONCLUSIONS
  These data show that BE and Adc of the esophagus and cardia have a similar phenotype and support the hypothesis that most of these tumors probably originate from preexisting BE.
authors.affiliation: Cirurgia Geral I, Department of Surgery, Instituto Português de Oncologia de Francisco Gentil, Centro de Lisboa, Portugal. Jose.CM.Almeida@mail.telepac.pt
authors.forename: J C
authors.initials: JC
authors.lastname: Mendes de Almeida
authors.forename: P
authors.initials: P
authors.lastname: Chaves
authors.forename: A D
authors.initials: AD
authors.lastname: Pereira
authors.forename: N K
authors.initials: NK
authors.lastname: Altorki
mesh_terms: D000230:Adenocarcinoma / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D000951:Antigens, Neoplasm / Q000378:metabolism*; D001471:Barrett Esophagus / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D014408:Biomarkers, Tumor / Q000378:metabolism*; D002471:Cell Transformation, Neoplastic / Q000378:metabolism; D004938:Esophageal Neoplasms / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D004942:Esophagitis, Peptic / Q000378:metabolism / Q000473:pathology; D019084:Fluorescent Antibody Technique, Indirect; D006651:Histocytochemistry; D006801:Humans; D009092:Mucous Membrane / Q000378:metabolism / Q000473:pathology; D010641:Phenotype; D013394:Sucrase-Isomaltase Complex / Q000378:metabolism*
chemical_list: D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; D013394:Sucrase-Isomaltase Complex