Progression of signet ring cell carcinomas in the human stomach

Sugihara, Hiroyuki; Hattori, Takanori; Fukuda, M; Katsura, Kanade; Fujita, Setsuya

doi:10.1002/1097-0142(19930315)71:6<1938::aid-cncr2820710603>3.0.co;2-w

Cited by 19 publications

(16 citation statements)

References 20 publications

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“…Another merit of static cytofluorometry is an ability to detect small polyploid populations that cannot be detected by the usual flow-cytometric analysis. It is important to distinguish DNA diploidy with polyploidy from that without polyploidy because the presence of polyploidy is also considered to reflect chromosomal instability, possibly reflecting near-diploid aneuploidy at the chromosome level [29].…”

Section: Discussionsupporting

confidence: 92%

Different roles of p53 between Epstein-Barr virus-positive and -negative gastric carcinomas of matched histology

et al. 2001

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To clarify the role of p53 in the development of Epstein-Barr virus (EBV)-associated gastric carcinoma, we examined DNA-ploidy pattern, the immunoreactivity of p53, p21(WAF1) and Ki-67 and the incidence of mitosis and apoptosis in EBV-positive and -negative gastric carcinomas of similar histology: a lace pattern and/or gastric carcinoma with lymphoid stroma. There was no significant difference in DNA-ploidy pattern, Ki-67 index or frequencies of mitosis and apoptosis between the two groups. In deeply invasive tumours (involving the muscularis propria or deeper), p53-positive ones were rare in the EBV-encoded small RNA (EBER)-positive group and very common in the EBER-negative group, while in superficial tumours, around one-half of them were p53-positive in both groups. In p53-positive superficial tumours, p21(WAF1)-positive ones accounted for 80% in the EBER-positive group and were scarce in the EBER-negative group. It is thus possible that p53 immunoreactivity reflects the overexpression of wild-type p53 and the stabilization of mutant p53 in the EBER-positive and -negative groups, respectively. The role of p53 in tumour development seems to be smaller in EBER-positive than in -negative gastric carcinomas.

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Section: Discussionsupporting

confidence: 92%

Different roles of p53 between Epstein-Barr virus-positive and -negative gastric carcinomas of matched histology

et al. 2001

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“…One candidate we have examined is the DNA-ploidy pattern, because it seemed very important to examine quantitative change of DNA to study a mechanism of oncogene amplification at an earlier stage. In addition, the occurrence of both DNA-aneuploidy and DNA-polyploidy has been reported by us to correlate with the progression of gastric cancer [12,13,28]. The Table 2 DNA ploidy pattern (with polyploidy) of gastric cancers studied& / t b l .…”

Section: Discussionmentioning

confidence: 89%

“…We consider that it is important to detect polyploidy to know about chromosome instability in the tumour, because polyploidy is detected quite commonly in DNA-aneuploid tumours but not in the normal gastric mucosa [12,28]. Furthermore, there is experimental and clinical evidence that polyploidization precedes the occurrence of DNA-aneuploidy and further evolution of new stemlines from the DNA-aneuploid cell population during tumour progression [6,9,21,27].…”

Section: Discussionmentioning

confidence: 99%

Amplification of growth factor receptor genes and DNA ploidy pattern in the progression of gastric cancer

et al. 1997

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To study the background of oncogene amplification in gastric cancers, we examined the correlation between occurrence of oncogene amplification and DNA ploidy pattern. In 57 primary gastric cancers, amplifications of c-erbB, c-erbB-2, c-met and K-sam genes were investigated by Southern blot analysis, and the DNA ploidy pattern was determined by static cytofluorometry and by flow cytometry. Oncogene amplification was detected in 11 cancers, 10 of which were advanced gastric cancers and 1 was an early differentiated type. The amplification of c-erbB-2 and K-sam genes was found exclusively in differentiated- and undifferentiated-type cancers, respectively. Of the 11 cancers, 5 were DNA-diploid and 6 were DNA-aneuploid. All the 11 tumours with oncogene amplification contained polyploid cell populations (polyploidy), whereas none of the tumours without polyploidy showed oncogene amplification. In differentiated-type cancers the incidence of polyploidy was high in both early and advanced stages, while in undifferentiated-type cancers it was low in early stages but significantly higher in advanced stages. It was shown that amplification of growth factor receptor genes is closely related to the presence of polyploidy, irrespective of any different stemline DNA-ploidy mode. The time-course of oncogene amplification and kinds of genes amplified may differ between differentiated- and undifferentiated-type gastric cancers.

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“…The mapping of DNA ploidy in individual tumors demonstrated that intramucosal spreading growth is characteristic of DNA-diploid tumor cells of this type and that the appearance of a DNA-aneuploid subclone is closely related to enhanced chromosomal instability and deeply invasive growth [23]. Such subclones are reported to occur in a stochastic rather than a time-dependent manner [24]. It may be because the occurrence of a subclone with an enhanced growth advantage is a much rarer event than the occurrence of a neutral subclone with changes in mucin phenotype.…”

Section: Discussionmentioning

confidence: 99%

Time-dependent expression of intestinal phenotype in signet ring cell carcinomas of the human stomach

et al. 2001

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Signet ring cell carcinomas of the stomach are thought to arise from the proper gastric mucosa without intestinal metaplasia. It was recently reported that intestinal phenotypes appear along with tumor progression. In this study, we performed several experiments to reconsider the significance of this intestinalization in the growth of signet ring cell carcinoma. We applied mucin histochemistry with monoclonal antibodies MUC2 (Ccp58) and M1 (45M1), and paradoxical concanavalin A staining for class III mucin [PCS(III)] reaction to 29 intramucosal and 25 deeply invasive carcinomas of this type and correlated the phenotypic expression with the size of the mucosal spread and the depth of tumor invasion. It was found that the larger the size of the mucosal lesion, the more frequently the intestinal phenotypes were demonstrated. There was no significant increase in the expression of the intestinal phenotype as the tumor invaded the deeper part of the mucosa or as the intestinal metaplasia increased in the background mucosa. The intestinal expression appeared to be suppressed in the earlier phase of deep invasion. In the mucosal part of the tumor, the intestinal phenotype was often expressed regionally and incompletely, coexisting with gastric phenotypes at the cellular and the tissue levels. These findings indicate that the expression of the intestinal phenotype is a time-dependent and unstable phenomenon probably based on the accumulation of genetic changes and plays a neutral role in progression of signet ring cell carcinomas.

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Progression of signet ring cell carcinomas in the human stomach

Cited by 19 publications

References 20 publications

Different roles of p53 between Epstein-Barr virus-positive and -negative gastric carcinomas of matched histology

Different roles of p53 between Epstein-Barr virus-positive and -negative gastric carcinomas of matched histology

Amplification of growth factor receptor genes and DNA ploidy pattern in the progression of gastric cancer

Time-dependent expression of intestinal phenotype in signet ring cell carcinomas of the human stomach

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