Preferential up-regulation of heparanase and cyclooxygenase-2 in carcinogenesis of Barrett's oesophagus and intestinal-type gastric carcinoma

Histopathology. 2010 Jul;57(1):90-100. doi: 10.1111/j.1365-2559.2010.03594.x.

Abstract

Aims: 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.

Methods and 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.

MeSH terms

  • Adenocarcinoma / blood supply
  • Adenocarcinoma / enzymology*
  • Adenocarcinoma / genetics
  • Adenocarcinoma / pathology
  • Barrett Esophagus / enzymology*
  • Barrett Esophagus / genetics
  • Barrett Esophagus / pathology
  • Base Sequence
  • Carcinoma in Situ / enzymology
  • Carcinoma in Situ / genetics
  • Carcinoma in Situ / pathology
  • Cell Line, Tumor
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism*
  • DNA Primers / genetics
  • Esophageal Neoplasms / blood supply
  • Esophageal Neoplasms / enzymology*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / pathology
  • Glucuronidase / genetics
  • Glucuronidase / metabolism*
  • Humans
  • Microvessels / pathology
  • Neovascularization, Pathologic
  • RNA, Messenger / genetics
  • RNA, Neoplasm / genetics
  • Stomach Neoplasms / enzymology*
  • Stomach Neoplasms / pathology
  • Up-Regulation

Substances

  • DNA Primers
  • RNA, Messenger
  • RNA, Neoplasm
  • Cyclooxygenase 2
  • heparanase
  • Glucuronidase