Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA.
Breast Cancer Res. 2011 Sep 7;13(5):314. doi: 10.1186/bcr2918.
The hereditary breast and ovarian cancer predisposition genes BRCA1 and BRCA2 account for the lion's share of heritable breast cancer risk in the human population. Loss of function of either gene results in defective homologous recombination (HR) and triggers genomic instability, accelerating breast tumorigenesis. A long-standing hypothesis proposes that BRCA1 and BRCA2 mediate HR following attempted replication across damaged DNA, ensuring error-free processing of the stalled replication fork. A recent paper describes a new replication fork protective function of BRCA2, which appears to collaborate with its HR function to suppress genomic instability.
遗传性乳腺癌和卵巢癌易感基因 BRCA1 和 BRCA2 占人类遗传性乳腺癌风险的绝大部分。这两个基因的功能丧失会导致同源重组（HR）缺陷，并引发基因组不稳定性，加速乳腺癌的发生。一个长期存在的假说提出，BRCA1 和 BRCA2 在试图跨越受损 DNA 进行复制后介导 HR，从而确保停滞的复制叉得到无差错的处理。最近的一篇论文描述了 BRCA2 的新复制叉保护功能，它似乎与 HR 功能合作，抑制基因组不稳定性。
