Bamba M, Sugihara H, Kushima R, Okada K, Tsukashita S, Horinouchi M, Hattori T
Department of Pathology, Shiga University of Medical Science, Ohtsu, Japan.
Virchows Arch. 2001 Jan;438(1):49-56. doi: 10.1007/s004280000307.
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.
胃印戒细胞癌被认为起源于没有肠化生的胃固有黏膜。最近有报道称，随着肿瘤进展会出现肠型表型。在本研究中，我们进行了多项实验，以重新审视这种肠化生在印戒细胞癌生长中的意义。我们将MUC2（Ccp58）和M1（45M1）单克隆抗体的黏液组织化学以及针对III类黏液的伴刀豆球蛋白A反常染色[PCS(III)]反应应用于29例这种类型的黏膜内癌和25例浸润性癌，并将表型表达与黏膜扩散大小和肿瘤浸润深度相关联。结果发现，黏膜病变越大，肠型表型出现的频率越高。随着肿瘤侵犯黏膜更深层或背景黏膜中肠化生增加，肠型表型的表达没有显著增加。在深度浸润的早期阶段，肠型表达似乎受到抑制。在肿瘤的黏膜部分，肠型表型常呈区域性且不完全表达，在细胞和组织水平上与胃型表型共存。这些发现表明，肠型表型的表达是一种可能基于基因变化积累的时间依赖性和不稳定现象，在印戒细胞癌进展中起中性作用。
