title: Effects of Helicobacter pylori infection on mucin expression in gastric carcinoma and pericancerous tissues.
abstract: BACKGROUND
  Helicobacter pylori infection is one of the major causes of human gastric carcinoma and can disturb the gastric mucosa barrier. Mucins have not only lubricating and protecting functions, but are also related to signal transduction, turnover of gastric epithelium and carcinogenesis of gastric mucosa. The aim of this study was to investigate the relationship between H. pylori infection and aberrant mucin expression in patients with gastric carcinoma.
  
  
  METHODS
  H. pylori infection was diagnosed by the Warthin-Starry staining method. Different kinds of mucins were detected using an immunohistochemical method.
  
  
  RESULTS
  Of 46 patients with gastric carcinoma, there were 26 patients who had H. pylori infection (56.5%). Of 21 pericancerous mucosas from the H. pylori-positive patients, 14 had MUC2 expression (66.7%), seven had strong MUC1 expression (+ + +) (33.7%), seven had strong MUC6 expression (+ + +) (33.3%), and five had strong MUC5AC expression (+ + +) (23.8%). In contrast, only six of 18 H. pylori-negative pericancerous mucosas had MUC2 expression (33.3%) (P < 0.05 compared with H. pylori-positive pericancerous mucosas), 12 had strong MUC1 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (75%) (P < 0.05), 11 had strong MUC6 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (68.8%) (P < 0.05), and 10 had strong MUC5AC expression (+ + +) in 14 H. pylori-negative pericancerous mucosas (71.4%) (P < 0.01). Of the H. pylori-positive cancerous tissues, 50% (13/26) had MUC1 expression and 38.5% (10/26) had MUC6 expression. In comparison, of the H. pylori-negative cancerous tissues, 80% (16/20) had MUC1 expression (P < 0.05) and 80% (16/20) had MUC6 expression (P < 0.01).
  
  
  CONCLUSIONS
  The results indicate that H. pylori infection can alter the expression of some mucin genes in pericancerous mucosa and cancerous tissues of gastric carcinoma, then destroy the gastric mucosa barrier.
authors.affiliation: Department of Gastroenterology, Southwestern Hospital, Third Military Medical University, Chongqing, China. rongquanw@hotmail.com
authors.forename: Rong-Quan
authors.initials: RQ
authors.lastname: Wang
authors.forename: Dian-Chun
authors.initials: DC
authors.lastname: Fang
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000032:analysis; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism; D002277:Carcinoma / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004273:DNA, Neoplasm / Q000235:genetics*; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic; D016481:Helicobacter Infections / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology / Q000302:isolation & purification; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009077:Mucins / Q000096:biosynthesis / Q000235:genetics*; D013274:Stomach Neoplasms / Q000378:metabolism* / Q000473:pathology
chemical_list: D000907:Antibodies, Bacterial; D014408:Biomarkers, Tumor; D004273:DNA, Neoplasm; D009077:Mucins