TY - JOUR
T1 - Gastric phenotypic expression and histogenesis of metachronous gastric cancers endoscopically resected
AU - Mizoshita, Tsutomu
AU - Kataoka, Hiromi
AU - Tanida, Satoshi
AU - Sasaki, Makoto
AU - Ogasawara, Naotaka
AU - Kubota, Eiji
AU - Wada, Tsuneya
AU - Yamada, Tomonori
AU - Mon, Yoshinori
AU - Shimura, Takaya
AU - Tsukamoto, Tetsuya
AU - Tatematsu, Masae
AU - Joh, Takashi
PY - 2009/3
Y1 - 2009/3
N2 - Background/Aims: Endoscopic Resection (ER) has been performed for early gastric cancers, and metachronous gastric cancers (MGCs) were occasionally observed. Most MGCs were classified histologically as the differentiated type. However, there have been no data on the gastric and intestinal phenotypic classification of MGCs. In our previous study, Hp-infection in MG may trigger intestinalization of gastric cancers. We therefore speculate the phenotype shift in MGC lesions under Hp- chronic-infection. Methodology: We examined the 17 MGC lesions phenotypieally and histologically by using several gastric and intestinal epithelial cell markers, MUC5AC, MUC6, MUC2 and villin. Results: Most lesions (16/17) exhibited the differentiated type. In 8 first cancers, the lesions were divided phenotypically into 2 0, 4 01, 1 I, and 1 N types. In 9 second/third cancers, the lesions were divided phenotypically into 3 G, 1 01, 4 I, and 1 N types. The first lesions (6/8) had more gastric phenotypic expression compared with the second/third ones (4/9) in the MGCs, although there was no significant difference between two groups (1O.28). Conclusion: Our present data suggest the possibility that the cancer retaining G type is detected endoscopically earlier than that obtaining the intestinal phenotypic expression by the phenotypic shift, which may partially explain the MGC occurrence.
AB - Background/Aims: Endoscopic Resection (ER) has been performed for early gastric cancers, and metachronous gastric cancers (MGCs) were occasionally observed. Most MGCs were classified histologically as the differentiated type. However, there have been no data on the gastric and intestinal phenotypic classification of MGCs. In our previous study, Hp-infection in MG may trigger intestinalization of gastric cancers. We therefore speculate the phenotype shift in MGC lesions under Hp- chronic-infection. Methodology: We examined the 17 MGC lesions phenotypieally and histologically by using several gastric and intestinal epithelial cell markers, MUC5AC, MUC6, MUC2 and villin. Results: Most lesions (16/17) exhibited the differentiated type. In 8 first cancers, the lesions were divided phenotypically into 2 0, 4 01, 1 I, and 1 N types. In 9 second/third cancers, the lesions were divided phenotypically into 3 G, 1 01, 4 I, and 1 N types. The first lesions (6/8) had more gastric phenotypic expression compared with the second/third ones (4/9) in the MGCs, although there was no significant difference between two groups (1O.28). Conclusion: Our present data suggest the possibility that the cancer retaining G type is detected endoscopically earlier than that obtaining the intestinal phenotypic expression by the phenotypic shift, which may partially explain the MGC occurrence.
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M3 - Article
C2 - 19579639
AN - SCOPUS:67649201140
SN - 0172-6390
VL - 56
SP - 542
EP - 546
JO - Hepato-gastroenterology
JF - Hepato-gastroenterology
IS - 90
ER -