Gastric and Intestinal Phenotypic Expression of Human Stomach Cancers as Revealed by Pepsinogen lmmunohistochemistry and Mucin Histochemistry

Tatematsu, Masae; Ichinose, Masakazu; Miki, Kazumasa; Hasegawa, Ryohei; Katô, Toshio; Ito, Nobuyuki

doi:10.1111/j.1440-1827.1990.tb01591.x

Cited by 125 publications

(189 citation statements)

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“…b P ¼ 0.0493 (advanced adenocarcinoma of the gastric cardia vs advanced adenocarcinoma of the distal stomach) and P ¼ 0.0363 (total adenocarcinoma of the gastric cardia vs total adenocarcinoma of the distal stomach). Table 5 Genetic alterations in differentiated-type adenocarcinoma of the gastric cardia and distal stomach whereas I-phenotype tumours have been reported to account for 10.1% of all undifferentiated-type tumours (Tatematsu et al, 1990;Egashira et al, 1999;Tajima et al, 2001aTajima et al, , b, 2004Yamazaki et al, 2006). These previous data suggest that gastric carcinomas may arise from various types of gastric mucosa, although differentiatedtype tumours have generally been considered to arise from gastric mucosa with intestinal metaplasia and undifferentiated-type tumours to arise from ordinary gastric mucosa without intestinal metaplasia (Lauren 1965;Nakamura et al, 1968).…”

Section: Discussionmentioning

confidence: 99%

Differences in the histological findings, phenotypic marker expressions and genetic alterations between adenocarcinoma of the gastric cardia and distal stomach

et al. 2007

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Adenocarcinoma of the gastric cardia (C-Ca) is possibly a specific subtype of gastric carcinoma. The purpose of this study was to clarify the differences in the clinicopathological characteristics between C-Ca and adenocarcinoma of the distal stomach (D-Ca), and also the differences in the expressions of gastric and intestinal phenotypic markers and genetic alterations between the two. The clinicopathological findings in 72 cases with C-Ca were examined and compared with those in 170 cases with D-Ca. The phenotypic marker expressions examined were those of human gastric mucin (HGM), MUC6, MUC2 and CD10. Furthermore, the presence of mutations in the APC, K-ras and p53 genes and the microsatellite instability status of the tumour were also determined. C-Ca was associated with a significantly higher incidence of differentiated-type tumours and lymphatic vessel invasion (LVI) as compared with D-Ca (72.2 vs 48.2%, P ¼ 0.0006 and 72.2 vs 55.3%, P ¼ 0.0232, respectively). Oesophageal invasion by the tumour beyond the oesophago-gastric junction (OGJ) was found in 56.9% of cases with C-Ca; LVI in the area of oesophageal invasion was demonstrated in 61% of these cases. Also, LVI was found more frequently in cases of C-Ca with oesophageal invasion than in those without oesophageal invasion (82.9 vs 58.1%, P ¼ 0.0197). The incidence of undifferentiated-type tumours was significantly higher in cases with advanced-stage C-Ca than in those with early-stage C-Ca (5 vs 36.5%, P ¼ 0.0076). A significantly greater frequency of HGM expression in early-stage C-Ca and significantly lower frequency of MUC2 expression in advanced-stage C-Ca was observed as compared with the corresponding values in cases of D-Ca (78.9 vs 52.2%, P ¼ 0.0402 and 51.5 vs 84.6%, P ¼ 0.0247, respectively). Mutation of the APC gene was found in only one of all cases of C-Ca, and the frequency of mutation of the APC gene was significantly lower in cases of C-Ca than in those of D-Ca (2.4 vs 20.0%, P ¼ 0.0108). The observations in this study suggest that C-Ca is a more aggressive tumour than D-Ca. The differences in biological behavior between C-Ca and D-Ca may result from the different histological findings in the wall of the OGJ and the different genetic pathways involved in the carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Differences in the histological findings, phenotypic marker expressions and genetic alterations between adenocarcinoma of the gastric cardia and distal stomach

et al. 2007

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“…[29][30][31][32][33] By sequential observation of rat glandular stomach carcinomas and comparisons of phenotypic expression of human gastric carcinoma cells between early and advanced cases, a phenotypic shift from gastric to intestinal epithelial cell type expression has been recognized with progression of each histological type of gastric carcinomas. [33][34][35][36] The present results regarding phenotypic expression of tumor cells showed that mouse glandular stomach adenomas and carcinomas consist solely of tumor cells of gastric epithelial cell type, without any intestinal metaplasia in the mucosa surrounding carcinomas.…”

Section: Discussionmentioning

confidence: 99%

N‐Methyl‐N‐nitrosourea Concentration‐dependent, Rather than Total Intake‐dependent, Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice

Yamachika

Nakanishi

Inada

et al. 1998

Japanese Journal of Cancer Research

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The influence of the level of carcinogen exposure on histopathological types and cellular differentiation of the induced tumors was examined in 100 male BALB/c mice given N-methyl-Nnitrosourea (MNU) in their drinking water at 240 ppm on alternate weeks (total exposure: five weeks) (group 1), at 120 ppm similarly (total exposure: ten weeks) (group 2), at 60 ppm for 20 weeks continuously (group 3), or at 30 ppm for 40 weeks continuously (group 4). Forty-three differentiated and 17 undifferentiated type adenocarcinomas were induced. Glandular stomach carcinomas and undifferentiated type lesions were more common in mice treated with a high concentration of MNU for a short period than with a low concentration of MNU for a long period, even though total measured intake of MNU was smaller (P< < < <0.01). All the induced glandular stomach carcinomas, independent of the treatment schedule, consisted entirely of gastric phenotype cells. In conclusion, the induction of glandular stomach cancers and the proportion of undifferentiated type lesions depend not on the total quantity, but rather on the concentration of the carcinogen, while the phenotypic expression of tumor cells is not affected by the differences in the administration protocol.

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“…We have shown [2][3][4][5] that human and rat gastric cancer cells of different histologic types can be classified into 2 categories: a gastric epithelial cell type, comprising pyloric gland cells and surface mucous cells, and an intestinal epithelial cell type, comprising goblet cells and intestinal absorptive cells, based on our recent results obtained by mucin histochemistry [paradoxical concanavalin A (Con A), galactose oxidase Schiff (GOS), and sialidase-GOS staining] and enzyme immunohistochemistry [pepsinogen staining].…”

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“…In contrast, no ALP was detectable in normal gastric mucosae except for the I-ALP activity in intestinal metaplasias. We have reported 16) relatively low contents of ALPs in 13 out of 38 human primary signet-ring cell carcinomas. Other authors 6,17) have also demonstrated a low level of ALP expression in various human gastric carcinomas.…”

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Increased Expression of Sucrase and Intestinal‐type Alkaline Phosphatase in Human Gastric Carcinomas with Progression

Nakamura

Inada

Hirano

et al. 1998

Japanese Journal of Cancer Research

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The activities of sucrase, total alkaline phosphatase (total ALP) and intestinal-type alkaline phosphatase (I-ALP) were assayed in gastric carcinomas and in their surrounding mucosae from 57 patients with advanced cancers, and the localization of sucrase in 203 carcinomas, including 86 early cancers, was examined immunohistochemically using polyclonal anti-sucrase antibody. All three enzymes were active in the 57 carcinomas as well as in their surrounding mucosae, but the levels were fairly low as compared to those in normal jejunum mucosa. A considerable part of the total ALP activity in tumor specimens was assumed to be due to I-ALP itself. Increased sucrase and I-ALP were found with greater depth of invasion by undifferentiated-type carcinomas. The pattern of immunohistochemical localization of sucrase in the 203 carcinomas also clearly indicated increased expression with greater depth of invasion even in differentiated-type carcinomas.

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Gastric and Intestinal Phenotypic Expression of Human Stomach Cancers as Revealed by Pepsinogen lmmunohistochemistry and Mucin Histochemistry

Cited by 125 publications

References 19 publications

Differences in the histological findings, phenotypic marker expressions and genetic alterations between adenocarcinoma of the gastric cardia and distal stomach

Differences in the histological findings, phenotypic marker expressions and genetic alterations between adenocarcinoma of the gastric cardia and distal stomach

N‐Methyl‐N‐nitrosourea Concentration‐dependent, Rather than Total Intake‐dependent, Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice

Increased Expression of Sucrase and Intestinal‐type Alkaline Phosphatase in Human Gastric Carcinomas with Progression

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