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结直肠癌发生过程中非整倍体与p53过表达之间的关系。

The relationship between aneuploidy and p53 overexpression during genesis of colorectal adenocarcinoma.

作者信息

Auer G U, Heselmeyer K M, Steinbeck R G, Munck-Wikland E, Zetterberg A D

机构信息

Department of Tumour Pathology, Karolinska Institute and Hospital, Stockholm, Sweden.

出版信息

Virchows Arch. 1994;424(4):343-7. doi: 10.1007/BF00190554.

Abstract

This paper describes the investigation of nuclear DNA content and p53 immunoreactivity in normal mucosa (n = 25), mildly (n = 15), moderately (n = 28) and severely atypical (n = 22) colorectal adenomas and in colorectal adenocarcinomas (n = 116). Twenty-seven per cent of the mildly atypical, 43% of the moderately, 77% of the severely atypical adenomas and 91% of the colorectal carcinomas were distinctly aneuploid. In the aneuploid lesions p53 immunoreactivity was not observed in mildly atypical adenomas, whereas 17% of the moderately atypical, 24% of the severely atypical adenomas and 66% of the adenocarcinomas were p53 positive. None of the diploid lesions were p53 immunoreactive. These data are interpreted to indicate that genomic instability as reflected by crude aneuploidy occurs early during genesis of colorectal carcinoma and represents a high risk factor for p53-gene mutation.

摘要

本文描述了对正常黏膜(n = 25)、轻度(n = 15)、中度(n = 28)和重度非典型(n = 22)大肠腺瘤以及大肠腺癌(n = 116)的核DNA含量和p53免疫反应性的研究。27%的轻度非典型腺瘤、43%的中度腺瘤、77%的重度非典型腺瘤和91%的大肠腺癌明显为非整倍体。在非整倍体病变中,轻度非典型腺瘤未观察到p53免疫反应性,而17%的中度非典型腺瘤、24%的重度非典型腺瘤和66%的腺癌为p53阳性。所有二倍体病变均无p53免疫反应性。这些数据被解释为表明,粗略的非整倍体所反映的基因组不稳定性在大肠癌发生早期就已出现,并且是p53基因突变的高风险因素。

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