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结肠小广基锯齿状腺瘤/息肉(SSA/P)中发生的腺癌:8例病变的临床病理研究

Adenocarcinoma arising in small sessile serrated adenoma/polyp (SSA/P) of the colon: clinicopathological study of eight lesions.

作者信息

Ban Shinichi, Mitomi Hiroyuki, Horiguchi Hisashi, Sato Hideaki, Shimizu Michio

机构信息

Department of Pathology, Saiseikai Kawaguchi General Hospital, Kawaguchi, Japan.

出版信息

Pathol Int. 2014 Mar;64(3):123-32. doi: 10.1111/pin.12147.

DOI:10.1111/pin.12147
PMID:24698422
Abstract

We reviewed the clinicopathological findings of eight cases of sessile serrated adenoma/polyps (SSA/Ps) with carcinoma, the largest diameter of which was 10 mm or less. All lesions were polyps located in the right side of the colon. Four lesions showed submucosal invasion and one lesion invaded the proper muscle layer. The depth of invasion, however, did not seem to be related to the carcinoma area size. Most carcinomas were well to moderately differentiated tubular adenocarcinomas focally showing some serrated appearances, and the predominant component of one carcinoma was a poorly differentiated medullary growth with inflammatory stroma. Rapid progression to invasive carcinoma from SSA/P was suggested for the carcinoma with proper muscle invasion whereas one submucosally invasive carcinoma was considered to progress over 7 years. Immunohistochemically, it was suggested that with or without hMLH1 protein loss, alterations of p53 and/or Wnt signaling pathway can be involved in the cancerization through SSA/Ps. The carcinomas irregularly imitated the mucin expression of the SSA/Ps (positive for MUC5AC and MUC2, and MUC6 expression in crypt bases), which was lost with progression of the carcinomas. Analyses of small SSA/P lesions with cancerization would facilitate the understanding of the mode of progression of SSA/Ps and their early detection.

摘要

我们回顾了8例直径最大为10毫米或更小的伴有癌的无蒂锯齿状腺瘤/息肉(SSA/P)的临床病理特征。所有病变均为位于结肠右侧的息肉。4个病变显示黏膜下浸润,1个病变侵犯固有肌层。然而,浸润深度似乎与癌灶大小无关。大多数癌为高分化至中分化管状腺癌,局部可见一些锯齿状外观,1例癌的主要成分是伴有炎性间质的低分化髓样生长。对于侵犯固有肌层的癌,提示SSA/P可快速进展为浸润性癌,而1例黏膜下浸润性癌被认为经过7年才进展。免疫组化显示,无论有无hMLH1蛋白缺失,p53和/或Wnt信号通路的改变可能参与SSA/P的癌变过程。癌不规则地模仿SSA/P的黏蛋白表达(MUC5AC和MUC2阳性,隐窝底部有MUC6表达),随着癌的进展这种表达会消失。对伴有癌变的小SSA/P病变进行分析将有助于理解SSA/P的进展模式及其早期检测。

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