Allellic HER-2 codon 655 polymorphism and the influence of plasma HER-2 levels in breast cancer Egyptian female patients

被引：2

作者：

Nassef A.A. ^{[1
]}

Ibrahim N.Y. ^{[2
]}

机构：

[1] Department of Clinical Pathology, Kasr Al-Ainy School of Medicine, Cairo University, Cairo

[2] Department of Medical Oncology, Kasr Al-Ainy School of Medicine, Cairo University, Cairo

来源：

Comparative Clinical Pathology | 2014年 / 23卷 / 3期

关键词：

Breast cancer; HER-2; 655; polymorphism; Plasma HER-2 level; Prognosis of cancer breast;

D O I：

10.1007/s00580-012-1658-4

中图分类号：

学科分类号：

摘要：

Breast cancer is the most common type of cancer and the most common cause of cancer-related mortality among women worldwide. Alterations of human epidermal growth factor receptor-2 (HER-2) proto-oncogene have been associated with carcinogenesis and poor prognosis of breast cancers. HER-2 DNA amplification is suggested to be the principal mechanism of HER-2 protein activation. The aim of the study was to clarify the possible association between HER-2 gene polymorphism at codon 655, free plasma HER-2 level, and breast cancer risk. Eighty Egyptian female patients (40 with early breast cancer and 40 with locally advanced breast cancer) were tested for HER-2 genetic polymorphism at codon 655 by restriction fragment length polymorphism-polymerase chain reaction assay. Also, the plasma level of HER-2 was measured using enzyme-linked immunosorbent assay. There was significant increase in mutant G allele frequency among locally advanced group compared to the control group and this conferred 12-fold increased disease risk among the studied group. No significant association could be detected between early breast cancer and HER-2 gene polymorphism. There is a statistically significant increase in the mean plasma HER-2 level among locally advanced breast cancer patients in comparison to the control group suggesting that plasma HER-2 contributes to the development, the higher stage, and dissemination of breast cancer. © 2012 Springer-Verlag London.

引用

页码：613 / 617

页数：4

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