RAD51是致癌基因，编码蛋白是RAD51重组酶家族的成员，其参与同源重组（HR）介导的双链DNA断裂修复（DSB）。RAD51在DSB的早期起作用：切除位于DSB断裂位点侧翼的5'端DNA链和单链突出端被RAD51包被形成核蛋白丝。RAD51与已知肿瘤抑制因子（BRCA1，BRCA2和PALB2）形成蛋白质复合物；具体而言，BRCA2在DNA双链断裂位点加载RAD51单体。RAD51胚系突变可能会增加某些人群的乳腺癌风险；而其他研究表明RAD51（135 G / C）单核苷酸多态性可能会增加BRCA2突变携带者的乳腺癌风险。RAD51在人类癌症中发生突变的频率很低；然而，RAD51过度表达与几种肿瘤类型（包括胰腺和乳腺癌）的致癌潜力增加有关。

RAD51 is a member of the RAD51 recombinase family that functions in homologous recombination (HR)-mediated repair of double-stranded DNA breaks (DSBs). RAD51 acts at an early step in the DSB pathway: the 5’ended DNA strands flanking the DSB break site are resected and the single-stranded overhangs are coated by RAD51 forming a nucleo-protein filament. RAD51 then probes for homologous DNA and initiates the process of strand invasion and exchange between homologous DNA. RAD51 forms protein complexes with known tumor suppressors including BRCA1, BRCA2 and PALB2; specifically, BRCA2 loads RAD51 monomers at sites of DNA double-strand breaks. RAD51 germline mutations may increase breast cancer risk in certain populations, while other studies suggest the RAD51 135 G/C single nucleotide polymorphism may increase breast cancer risk in BRCA2 mutation carriers. RAD51 is infrequently mutated in human cancer; however, RAD51 overexpression has been linked to increased oncogenic potential in several tumor types, including pancreatic and breast.

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