title: Expression of cyclooxygenase-2 in primary and remnant gastric carcinoma: comparing it with p53 accumulation, Helicobacter pylori infection, and vascular endothelial growth factor expression.
abstract: OBJECTIVE
  Cyclooxygenase-2 (COX-2) expression may contribute to the synthesis of prostanoids, which have been related to carcinogenesis and tumor progression. It is well known that the gastric remnant is at greater risk of the development of gastric cancer than is the whole stomach; incidence rates for gastric cardia adenocarcinoma are rising in the United States and Europe. Our objective was to determine the involvement of COX-2 in primary and remnant gastric cancer tissues as well as in adjacent noncancerous mucosa.
  
  
  METHODS
  We investigated the expression of COX-2 in 91 human gastric cancer tissue and adjacent noncancerous mucosa samples (40 remnant gastric cancer, 37 gastric cardia cancer, and 14 gastric corpus and antrum cancer), using immunohistochemistry. In addition, p53 expression, Helicobacter pylori infection, and vascular endothelial growth factor in the tissues were evaluated by immunohistochemical staining and compared with COX-2 expression.
  
  
  RESULTS
  There were no significant differences in clinicopathological data in the gastric cancer tissues. There was a significant relation between the expression of COX-2 and p53 in gastric cancer tissues (P = 0.0048). However, vascular endothelial growth factor expression and Helicobacter pylori infection showed no correlation with the expression of COX-2. In the case of adjacent noncancerous mucosa, the positive rate of COX-2 expression was significantly higher in the remnant gastric cancers (75.0%) than in the primary gastric cancers (25.5%) (P < 0.0001).
  
  
  CONCLUSIONS
  This information may help in the analysis of the carcinogenesis of gastric cancer; there is also a possibility that the COX-2 selective inhibitor to the remnant gastric cancer has a chemopreventive effect.
authors.affiliation: Department of Surgery and Surgical Basic Science, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kawabe
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Shimada
authors.forename: Shigeki
authors.initials: S
authors.lastname: Uchida
authors.forename: Masato
authors.initials: M
authors.lastname: Maeda
authors.forename: Seiji
authors.initials: S
authors.lastname: Yamasaki
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kato
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Hashimoto
authors.forename: Gakuji
authors.initials: G
authors.lastname: Ohshio
authors.forename: Masao
authors.initials: M
authors.lastname: Matsumoto
authors.forename: Masayuki
authors.initials: M
authors.lastname: Imamura
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002299:Cardia / Q000473:pathology; D051546:Cyclooxygenase 2; D016228:Endothelial Growth Factors / Q000096:biosynthesis*; D005260:Female; D016481:Helicobacter Infections / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000096:biosynthesis*; D008222:Lymphokines / Q000096:biosynthesis*; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D018365:Neoplasm, Residual; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis*; D013274:Stomach Neoplasms / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D007527:Isoenzymes; D008222:Lymphokines; D008565:Membrane Proteins; D016159:Tumor Suppressor Protein p53; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases