Jara Lilian, Acevedo Monica L, Blanco Rafael, Castro Victor G, Bravo Teresa, Gómez Fernando, Waugh Enrique, Peralta Octavio, Cabrera Elsa, Reyes José M, Ampuero Sandra, González-Hormazábal Patricio
Human Genetics Program, Institute of Biomedical Sciences (ICBM), School of Medicine, University of Chile, Av. Independencia 1027, P.O. Box 70061, Santiago, Chile.
Cancer Genet Cytogenet. 2007 Oct 1;178(1):65-9. doi: 10.1016/j.cancergencyto.2007.05.024.
Several studies have reported that mutations in genes involved in maintenance of genome integrity may be responsible for increased cancer risk. Human RAD51, known to function in DNA repair, interacts with a number of proteins implicated in breast cancer (BC), including BRCA1 and BRCA2. Few studies have investigated the role of RAD51 gene variations in familial BC. To detect potential novel gene defects that may contribute to hereditary BC susceptibility, 143 patients belonging to 143 Chilean families tested for BRCA1 and BRCA2 mutations were screened for mutations in RAD51, using conformational sensitive gel electrophoresis (CSGE) and DNA sequencing. No mutations were detected in the exon or splice-boundary regions of the RAD51 gene in these families. The RAD51 135G>C polymorphism (c.-98G>C, rs1801320) was studied in a case-control design, to evaluate its possible association with BC susceptibility. The frequency of the RAD51 135C allele was established in 143 cases and 247 controls, using restriction fragment length polymorphism-polymerase chain reaction. RAD51 135C genotypes (G/C and C/C) were associated with an increased BC risk only among women with (a) a family history of BC, (b) BRCA1/2 negative (n = 131), and (c) age at onset <50 years (P = 0.020; OR = 2.17, 95% CI = 1.11-4.24). Thus, we propose that RAD51 135G>C polymorphism presents an increased risk of familial BC in women with age < 50 years at diagnosis, and this polymorphism may be a BC risk variant. This finding should be confirmed in other populations.
多项研究报告称,参与维持基因组完整性的基因发生突变可能会增加患癌风险。已知人类RAD51在DNA修复中发挥作用,它与一些与乳腺癌(BC)相关的蛋白质相互作用,包括BRCA1和BRCA2。很少有研究调查RAD51基因变异在家族性BC中的作用。为了检测可能导致遗传性BC易感性的潜在新基因缺陷,我们对143个接受BRCA1和BRCA2突变检测的智利家族中的143名患者进行了RAD51突变筛查,采用构象敏感凝胶电泳(CSGE)和DNA测序技术。在这些家族的RAD51基因外显子或剪接边界区域未检测到突变。采用病例对照设计研究了RAD51 135G>C多态性(c.-98G>C,rs1801320),以评估其与BC易感性的可能关联。使用限制性片段长度多态性-聚合酶链反应确定了143例病例和247例对照中RAD51 135C等位基因的频率。RAD51 135C基因型(G/C和C/C)仅在具有以下特征的女性中与BC风险增加相关:(a)有BC家族史;(b)BRCA1/2阴性(n = 131);(c)发病年龄<50岁(P = 0.020;OR = 2.17,95%CI = 1.11 - 4.24)。因此,我们提出RAD51 135G>C多态性在诊断时年龄<50岁的女性中会增加家族性BC的风险,并且这种多态性可能是一种BC风险变异。这一发现应在其他人群中得到证实。