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甲状腺癌中葡萄糖转运蛋白1(GLUT1)、p63和p53的表达

Expression of the GLUT1 glucose transporter, p63 and p53 in thyroid carcinomas.

作者信息

Kim Youn Wha, Do In Gu, Park Yong-Koo

机构信息

Department of Pathology, School of Medicine, Kyung Hee University, #1 Hoiki-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.

出版信息

Pathol Res Pract. 2006;202(11):759-65. doi: 10.1016/j.prp.2006.07.006. Epub 2006 Oct 6.

DOI:10.1016/j.prp.2006.07.006
PMID:17029809
Abstract

Only few studies have evaluated the usefulness of the GLUT1 and p63 status of thyroid carcinomas in revealing tumorigenesis. We studied GLUT1, p53, and p63 immunoexpression in a total of 86 cases of various thyroid carcinoma types to determine the biological significance of GLUT1 and p63 expression in thyroid carcinomas. GLUT1 was detected in six cases of anaplastic carcinoma and in one case of poorly differentiated carcinoma with membranous staining. p63 was detected in five cases of anaplastic carcinoma, in one case of poorly differentiated carcinoma, and in five cases of papillary carcinoma with nuclear positivity. p53 was detected in six cases of anaplastic carcinoma, in one case of poorly differentiated carcinoma, and in one case of follicular carcinoma with nuclear positivity. Five of seven cases of anaplastic carcinoma expressed all three of these markers. The results suggest that GLUT1, p63, and p53 are not expressed in well-differentiated thyroid carcinomas, and that they are usually expressed late in the course of thyroid tumor progression. These data strongly suggest that in anaplastic carcinomas, impairment of p53-mediated repression results in increased GLUT1 and p63 expression, and that this probably reflects the differential regulation of hypoxia-responsive pathways and basal/stem cell regulatory pathways.

摘要

仅有少数研究评估了甲状腺癌中葡萄糖转运蛋白1(GLUT1)和p63状态在揭示肿瘤发生方面的作用。我们研究了86例不同类型甲状腺癌中GLUT1、p53和p63的免疫表达情况,以确定GLUT1和p63在甲状腺癌中表达的生物学意义。在6例间变性癌和1例低分化癌中检测到GLUT1呈膜性染色。在5例间变性癌、1例低分化癌和5例核阳性的乳头状癌中检测到p63。在6例间变性癌、1例低分化癌和1例核阳性的滤泡癌中检测到p53。7例间变性癌中有5例表达了所有这三种标志物。结果表明,GLUT1、p63和p53在高分化甲状腺癌中不表达,且它们通常在甲状腺肿瘤进展过程中晚期表达。这些数据强烈表明,在间变性癌中,p53介导的抑制作用受损导致GLUT1和p63表达增加,这可能反映了缺氧反应途径和基底/干细胞调节途径的差异调节。

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