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Preferential up‐regulation of heparanase and cyclooxygenase‐2 in carcinogenesis of Barrett’s oesophagus and intestinal‐type gastric carcinoma
Author(s) -
Sonoda Ryotaro,
Naomoto Yoshio,
Shirakawa Yasuhiro,
Fujiwara Yasuhiro,
Yamatsuji Tomoki,
Noma Kazuhiro,
Tanabe Shunsuke,
Takaoka Munenori,
Gunduz Mehmet,
Tsujigiwa Hidetsugu,
Nagatsuka Hitoshi,
Ohara Nobuya,
Yoshino Tadashi,
Takubo Kaiyo,
Vieth Michael,
Tanaka Noriaki
Publication year - 2010
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2010.03594.x
Subject(s) - heparanase , intestinal metaplasia , dysplasia , carcinogenesis , immunohistochemistry , medicine , pathology , cdx2 , adenocarcinoma , cancer , gastroenterology , in situ hybridization , metaplasia , carcinoma , cancer research , biology , metastasis , messenger rna , gene expression , biochemistry , homeobox , gene
Sonoda R, Naomoto Y, Shirakawa Y, Fujiwara Y, Yamatsuji T, Noma K, Tanabe S, Takaoka M, Gunduz M, Tsujigiwa H, Nagatsuka H, Ohara N, Yoshino T, Takubo K, Vieth M & Tanaka N
(2010) Histopathology 57 , 90–100
Preferential up‐regulation of heparanase and cyclooxygenase‐2 in carcinogenesis of Barrett’s oesophagus and intestinal‐type gastric carcinoma 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.