title: Preferential up-regulation of heparanase and cyclooxygenase-2 in carcinogenesis of Barrett's oesophagus and intestinal-type gastric carcinoma.
abstract: OBJECTIVE
  Metaplastic changes secondary to chronic inflammation at the gastro-oesophageal junction and at the pyloric antrum are recognized as the premalignant conditions of Barrett's oesophageal adenocarcinoma and intestinal-type gastric carcinoma (GC), respectively. Heparanase (HPSE) and cyclooxygenase (COX)-2 have been proved to play critical roles in inflammation as well as in cancer. The aim was to examine the meaning of their expression in inflammation-related carcinogenesis.
  
  
  RESULTS
  First, expression of HPSE and COX-2 in 78 clinical tissues of Barrett's oesophagus was examined by immunohistochemistry and in situ hybridization. Their expression was increased during the metaplasia-dysplasia sequence with increased neovascularization. Successively, their expression in Barrett's dysplasia was compared with that of GC (22 cases of diffuse-type and 10 of intestinal-type). Interestingly, the expression pattern in Barrett's dysplasia was similar to that in intestinal-type GC, which mainly arises from chronic inflammation. Furthermore, cultured cell lines isolated from differentiated GC tissues, which are often found to be of intestinal-type, revealed up-regulated mRNA expression of HPSE and COX-2.
  
  
  CONCLUSIONS
  HPSE and COX-2 are preferentially up-regulated in Barrett's oesophagus and intestinal-type GC. These molecules may play an important role during the development of inflammation-related adenocarcinoma of the upper gastrointestinal tract.
authors.affiliation: Department of Gastroenterological Surgery, Transplant, and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
authors.forename: Ryotaro
authors.initials: R
authors.lastname: Sonoda
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Naomoto
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Shirakawa
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Fujiwara
authors.forename: Tomoki
authors.initials: T
authors.lastname: Yamatsuji
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Noma
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Tanabe
authors.forename: Munenori
authors.initials: M
authors.lastname: Takaoka
authors.forename: Mehmet
authors.initials: M
authors.lastname: Gunduz
authors.forename: Hidetsugu
authors.initials: H
authors.lastname: Tsujigiwa
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Nagatsuka
authors.forename: Nobuya
authors.initials: N
authors.lastname: Ohara
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yoshino
authors.forename: Kaiyo
authors.initials: K
authors.lastname: Takubo
authors.forename: Michael
authors.initials: M
authors.lastname: Vieth
authors.forename: Noriaki
authors.initials: N
authors.lastname: Tanaka
mesh_terms: D000230:Adenocarcinoma / Q000098:blood supply / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D001471:Barrett Esophagus / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D001483:Base Sequence; D002278:Carcinoma in Situ / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D045744:Cell Line, Tumor; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism*; D017931:DNA Primers / Q000235:genetics; D004938:Esophageal Neoplasms / Q000098:blood supply / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D005966:Glucuronidase / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D055806:Microvessels / Q000473:pathology; D009389:Neovascularization, Pathologic; D012333:RNA, Messenger / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics; D013274:Stomach Neoplasms / Q000201:enzymology* / Q000473:pathology; D015854:Up-Regulation; D000099175:Heparanase
chemical_list: D051546:Cyclooxygenase 2; D017931:DNA Primers; D005966:Glucuronidase; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D000099175:Heparanase