Regulation and pharmacological targeting of RAD51 in cancer.

Regulation and pharmacological targeting of RAD51 in cancer.
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DOI:
10.1093/narcan/zcaa024
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发表时间:
2020-09
期刊:
影响因子:
5.1
通讯作者:
Bernstein KA
Bernstein KA
中科院分区:
其他
文献类型:
--
作者:
Grundy MK;Buckanovich RJ;Bernstein KA

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同源重组(HR)的调节是癌症预防的核心。然而,太少的HR会增加癌症的发病率,而太多的HR会导致癌症对治疗产生耐药性。重要的是,靶向HR缺陷的治疗方法在临床上显示出显著的疗效,可改善患者的预后,特别是乳腺癌和卵巢癌。RAD51是HR途径中DNA损伤修复的核心。因此,了解RAD51的功能和调控对癌症生物学至关重要。本综述将重点介绍RAD 51在癌症及其他疾病中的作用,以及如何将其功能的调节用作癌症治疗。
Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too much HR can drive cancer resistance to therapy. Importantly, therapeutics targeting HR deficiency have demonstrated a profound efficacy in the clinic improving patient outcomes, particularly for breast and ovarian cancer. RAD51 is central to DNA damage repair in the HR pathway. As such, understanding the function and regulation of RAD51 is essential for cancer biology. This review will focus on the role of RAD51 in cancer and beyond and how modulation of its function can be exploited as a cancer therapeutic.
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