title: Immunohistological study of cell cycle-related factors, oncogene expression, and cell proliferation in adenocarcinoma developed in Barrett's esophagus.
abstract: In addition to presenting clinicopathological findings in 3 patients with adenocarcinoma developed in Barrett's esophagus, we have investigated the expression of cell cycle-related factors, oncogenes and cell proliferation in normal squamous epithelium, specialized columnar epithelium (SCE) and adenocarcinoma in Barrett's esophagus, using immunohistological techniques. The expression of p21 in adenocarcinoma in Barrett's esophagus tended to be decreased in two mutated p53-strongly-positive patients and to be increased in one mutated p53-weakly-positive patient. Furthermore, mutated p53 was strongly expressed in the deep layer of the cancer, while p21 was expressed in the superficial layer of the cancer. Thus, mutated p53 was inversely correlated with p21 in adenocarcinoma in Barrett's esophagus. The mean positive cell rate (PR) of Ki-67 was 4% in normal squamous epithelium, 24.5% in the SCE, and 41.7% in the adenocarcinoma in Barrett's esophagus. The mean PR of proliferating cell nuclear antigen (PCNA) was 6% in normal squamous epithelium, 29.5% in the SCE, and 55% in the adenocarcinoma in Barrett's esophagus. Thus, the PR of Ki-67 and PCNA were clearly higher in the SCE in Barrett's esophagus than in normal squamous epithelium, indicating increased cell proliferation in the SCE in Barrett's esophagus. In conclusion, mutated p53 was inversely correlated with p21 in adenocarcinoma in Barrett's esophagus. p53 mutation and the expression of oncogenes such as c-erbB-2 and MDM2 were observed in the SCE in Barrett's esophagus, which showed higher cell proliferation than normal squamous epithelium, suggesting a high malignant potential of the SCE in Barrett's esophagus. We considered that it was important to carefully follow-up patients with Barrett's esophagus.
authors.affiliation: Department of Surgery, Kurume University School of Medicine, Kurume 830-0011, Japan. tfujii@med.kurume-u.ac.jp
authors.forename: Teruhiko
authors.initials: T
authors.lastname: Fujii
authors.forename: Shino
authors.initials: S
authors.lastname: Nakagawa
authors.forename: Mai
authors.initials: M
authors.lastname: Hanzawa
authors.forename: Susumu
authors.initials: S
authors.lastname: Sueyoshi
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Fujita
authors.forename: Kazuo
authors.initials: K
authors.lastname: Shirouzu
authors.forename: Hideaki
authors.initials: H
authors.lastname: Yamana
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D000368:Aged; D001471:Barrett Esophagus / Q000378:metabolism* / Q000473:pathology; D014408:Biomarkers, Tumor / Q000032:analysis / Q000378:metabolism*; D002455:Cell Division; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009363:Neoplasm Proteins / Q000378:metabolism*; D009687:Nuclear Proteins; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D051736:Proto-Oncogene Proteins c-mdm2; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D012680:Sensitivity and Specificity; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D014408:Biomarkers, Tumor; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D018809:Proliferating Cell Nuclear Antigen; D011518:Proto-Oncogene Proteins; D051736:Proto-Oncogene Proteins c-mdm2; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53; C493956:CDKN1A protein, human; C497206:MDM2 protein, human