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色素沉着病变中MLH1、MSH2、PMS1和PMS2表达降低表明随着恶性转化和肿瘤进展,DNA修复失败产物不断累积。

Decreased expression of MLH1, MSH2, PMS1 and PMS2 in pigmented lesions indicates accumulation of failed DNA repair along with malignant transformation and tumour progression.

作者信息

Korabiowska M, Dengler H, Kellner S, Stachura J, Schauer A

机构信息

UNIV GOTTINGEN,DEPT MED INFORMAT,D-37075 GOTTINGEN,GERMANY. JAGIELLONIAN UNIV,DEPT PATHOL,PL-31531 KRAKOW,POLAND.

出版信息

Oncol Rep. 1997 May-Jun;4(3):653-5. doi: 10.3892/or.4.3.653.

DOI:10.3892/or.4.3.653
PMID:21590118
Abstract

The tumorigenesis of human nonpolyposis colorectal cancer was reported to be connected with the mutations in DNA mismatch repair genes. The main aim of this study was to check the epression of 4 proteins MLH1, MSH2, PMS1 and PMS2 responsible for mismatch DNA repair in naevi and melanomas. Fifty-one naevi, 78 primary melanomas, 30 lymphatic and 7 organ melanoma metastases were stained for the presence of MLH1, MSH2, PMS1 and PMS2. All proteins were preserved in 88% of naevi and only in 37% of primary melanomas, 17% of lymphatic metastases and in none of the distant metastases. The difference of expression of all 4 proteins between naevi and melanomas was highly significant (p<0.01). MLH1 and MSH2 correlated significantly with each other as well with the follow-up of patients. On the basis of our results one can conclude that the defect of mismatch DNA repair plays an important role in both tumorigenesis of melanoma and metastatic spread of tumour.

摘要

据报道,人类非息肉病性结直肠癌的肿瘤发生与DNA错配修复基因的突变有关。本研究的主要目的是检测负责痣和黑色素瘤中DNA错配修复的4种蛋白质MLH1、MSH2、PMS1和PMS2的表达情况。对51个痣、78个原发性黑色素瘤、30个淋巴转移灶和7个器官黑色素瘤转移灶进行染色,以检测MLH1、MSH2、PMS1和PMS2的存在情况。所有蛋白质在88%的痣中得以保留,而在原发性黑色素瘤中仅为37%,在淋巴转移灶中为17%,在远处转移灶中则完全没有。痣和黑色素瘤之间所有4种蛋白质表达的差异具有高度显著性(p<0.01)。MLH1和MSH2之间以及与患者随访均显著相关。根据我们的结果可以得出结论,DNA错配修复缺陷在黑色素瘤的肿瘤发生和肿瘤转移扩散中均起重要作用。

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