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黑色素瘤肿瘤发生的遗传途径。

Genetic pathways to melanoma tumorigenesis.

作者信息

Hussein M R

机构信息

Department of Pathology, Assiut University Hospitals, Egypt.

出版信息

J Clin Pathol. 2004 Aug;57(8):797-801. doi: 10.1136/jcp.2003.015800.

DOI:10.1136/jcp.2003.015800
PMID:15280398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1770385/
Abstract

The incidence of cutaneous malignant melanomas is growing faster than that of any other cancer and therefore posing a major heath threat worldwide. In melanocytic skin tumours, the feasibility of correlating a specific pathological stage with a corresponding genetic alteration provides a remarkable opportunity to study the multistep tumorigenesis model. This multistep melanoma tumorigenesis is best described as a continuum of transformation of the melanocytes, melanocytic dysplasia, and melanoma formation. These steps involve genotypic alterations including loss of tumour suppressor genes, microsatellite instability, and alterations of the mismatch repair system. This review seeks to examine melanoma tumorigenesis based on these genetic changes.

摘要

皮肤恶性黑色素瘤的发病率增长速度比其他任何癌症都要快,因此在全球范围内构成了重大的健康威胁。在黑素细胞性皮肤肿瘤中,将特定病理阶段与相应基因改变相关联的可行性为研究多步骤肿瘤发生模型提供了一个难得的机会。这种多步骤黑色素瘤肿瘤发生过程最好被描述为黑素细胞转化、黑素细胞发育异常和黑色素瘤形成的连续过程。这些步骤涉及基因型改变,包括肿瘤抑制基因的缺失、微卫星不稳定性以及错配修复系统的改变。本综述旨在基于这些基因变化来研究黑色素瘤的肿瘤发生过程。

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Genetic pathways to melanoma tumorigenesis.黑色素瘤肿瘤发生的遗传途径。
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2
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本文引用的文献

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hMLH1 and hMSH2 gene mutations are present in radial growth-phase cutaneous malignant melanoma cell lines and can be induced further by ultraviolet-B irradiation.hMLH1和hMSH2基因突变存在于放射状生长期皮肤恶性黑色素瘤细胞系中,并且可通过紫外线B照射进一步诱导产生。
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Assessment of genetic instability in melanocytic skin lesions through microsatellite analysis of benign naevi, dysplastic naevi, and primary melanomas and their metastases.通过对良性痣、发育异常痣、原发性黑色素瘤及其转移灶进行微卫星分析,评估黑素细胞性皮肤病变中的基因不稳定性。
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Loss of heterozygosity, microsatellite instability, and mismatch repair protein alterations in the radial growth phase of cutaneous malignant melanomas.皮肤恶性黑色素瘤放射状生长期的杂合性缺失、微卫星不稳定性及错配修复蛋白改变
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