Perçinel Sibel, Savaş Berna, Ensari Arzu, Kuzu Işinsu, Kuzu M Ayhan, Bektaş Mehmet, Cetinkaya Hülya, Kurşun Nazmiye
Department of Pathology, Ankara University, School of Medicine, Ankara, Turkey.
Turk J Gastroenterol. 2007 Dec;18(4):230-8.
BACKGROUND/AIMS: Alterations in expression of mucins and aberrant expression of various types of mucin genes were observed in colorectal adenomas and carcinomas, though their significance in neoplastic transformation of colorectal epithelium is yet to be determined. The aim of this study was to determine expression of MUC1, MUC2, MUC5AC, and MUC6 through conventional adenoma-carcinoma sequence and polyps involved in the "serrated" pathway of the colorectum using tissue array technique.
In this study, a total of 172 cases including 100 colorectal polyps [8 hyperplastic polyps, 10 sessile serrated adenomas, 19 tubular, 37 tubulovillous, and 26 villous adenomas], 16 adenomas with intramucosal carcinoma, 28 conventional colorectal cancers, and 28 normal mucosae were examined. Tissue array blocks were prepared and sections were stained immunohistochemically for MUC1, MUC2, MUC5AC, and MUC6.
Expression of MUC1 significantly increased in close correlation with the neoplastic process and reached its highest values in intramucosal carcinomas and conventional colorectal cancers (p<0.001). In contrast, MUC2 expression showed a significant decrease in intramucosal carcinoma and conventional colorectal cancer groups (p<0.001). Sessile serrated adenomas exhibited the highest MUC5AC expression while adenomatous polyps showed an increase in MUC5AC expression in parallel with neoplastic progression (p<0.001). Hyperplastic polyps seemed to lie between normal mucosa and sessile serrated adenomas in terms of mucin expression, suggesting that they are morphologically and histogenetically linked.
Upregulation of MUC1 and MUC6 through the adenoma-carcinoma sequence together with downregulation of MUC2 and MUC5AC at the neoplastic end of the spectrum seem to follow the steps of malignant transformation.
背景/目的:在结直肠腺瘤和癌中观察到黏蛋白表达的改变以及各种类型黏蛋白基因的异常表达,但其在结直肠上皮肿瘤转化中的意义尚待确定。本研究的目的是使用组织芯片技术,通过传统的腺瘤-癌序列以及参与结直肠“锯齿状”途径的息肉来确定MUC1、MUC2、MUC5AC和MUC6的表达。
本研究共检查了172例病例,包括100例结直肠息肉[8例增生性息肉、10例无蒂锯齿状腺瘤、19例管状腺瘤、37例管状绒毛状腺瘤和26例绒毛状腺瘤]、16例伴有黏膜内癌的腺瘤、28例传统结直肠癌和28例正常黏膜。制备组织芯片块,并对切片进行MUC1、MUC2、MUC5AC和MUC6的免疫组织化学染色。
MUC1的表达与肿瘤发生过程密切相关,显著增加,在黏膜内癌和传统结直肠癌中达到最高值(p<0.001)。相比之下,MUC2的表达在黏膜内癌和传统结直肠癌组中显著降低(p<0.001)。无蒂锯齿状腺瘤表现出最高的MUC5AC表达,而腺瘤性息肉的MUC5AC表达随着肿瘤进展而增加(p<0.001)。增生性息肉在黏蛋白表达方面似乎介于正常黏膜和无蒂锯齿状腺瘤之间,表明它们在形态学和组织发生学上存在联系。
通过腺瘤-癌序列,MUC1和MUC6上调,同时在肿瘤谱系的末端MUC2和MUC5AC下调,似乎遵循了恶性转化的步骤。