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[共济失调毛细血管扩张症突变基因与乳腺癌易感性]

[Ataxia-telangiectasia mutated gene and breast cancer susceptibility].

作者信息

Zhang Nan, Che Jian, Bai Song, Wu Zheng, Cui Yuying, Zou Wei

机构信息

College of Life Science, Liaoning Normal University, Dalian 116029, China.

出版信息

Sheng Wu Gong Cheng Xue Bao. 2010 Jan;26(1):9-15.

PMID:20353086
Abstract

Breast cancer is bound up with the environment. As a consequence of DNA damage induced by environmental carcinogens, a number of sophisticated sensing and transduction systems are initiated and the signal is conveyed simultaneously to multiple effectors. This process ultimately results in cancer. The protein kinase Ataxia-telangiectasia mutated (ATM) that encoded by ATM gene is the master regulator of DNA damage response. In this consecutive reaction, the protein kinase ATM responds to the DNA damage by phosphorylating a variety of downstream substrates, which plays an important role in the inhibition of the development of breast cancer. After ATM gene mutate, DNA damaged could not be accurately repaired and finally accelerates breast cancer transformation and proliferation. With the further research of ATM gene structure, function and breast cancer susceptibility, the extensive attention is paid to the relationship between ATM gene and breast cancer susceptibility. We reviewed the research advances in breast cancer susceptibility in several aspects of ATM gene, including mutation, polymorphism and methylation.

摘要

乳腺癌与环境密切相关。由于环境致癌物诱导的DNA损伤,一系列复杂的传感和转导系统被启动,信号同时传递给多个效应器。这个过程最终导致癌症。由ATM基因编码的蛋白激酶共济失调毛细血管扩张突变蛋白(ATM)是DNA损伤反应的主要调节因子。在这个连续反应中,蛋白激酶ATM通过磷酸化多种下游底物来响应DNA损伤,这在抑制乳腺癌发展中起重要作用。ATM基因突变后,DNA损伤无法准确修复,最终加速乳腺癌的转化和增殖。随着对ATM基因结构、功能与乳腺癌易感性的进一步研究,ATM基因与乳腺癌易感性之间的关系受到广泛关注。我们从ATM基因的突变、多态性和甲基化等几个方面综述了乳腺癌易感性的研究进展。

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[Ataxia-telangiectasia mutated gene and breast cancer susceptibility].[共济失调毛细血管扩张症突变基因与乳腺癌易感性]
Sheng Wu Gong Cheng Xue Bao. 2010 Jan;26(1):9-15.
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