Hereditary Cancer Program, Catalan Institute of Oncology, ICO-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain.
Eur J Hum Genet. 2012 Dec;20(12):1256-64. doi: 10.1038/ejhg.2012.136. Epub 2012 Jul 4.
Recently, constitutional MLH1 epimutations have been identified in a subset of Lynch syndrome (LS) cases. The aim of this study was the identification of patients harboring constitutional MLH1 epimutations in a set of 34 patients with a clinical suspicion of LS, MLH1-methylated tumors and non-detected germline mutations in mismatch repair (MMR) genes. MLH1 promoter methylation was analyzed in lymphocyte DNA samples by MS-MLPA (Methylation-specific multiplex ligation-dependent probe amplification). Confirmation of MLH1 constitutional methylation was performed by MS-MCA (Methylation-specific melting curve analysis), bisulfite sequencing and pyrosequencing in different biological samples. Allelic expression was determined using heterozygous polymorphisms. Vertical transmission was evaluated by MS-MLPA and haplotype analyses. MS-MLPA analysis detected constitutional MLH1 methylation in 2 of the 34 individuals whose colorectal cancers showed MLH1 methylation (5.9%). These results were confirmed by bisulfite-based methods. Both epimutation carriers had developed metachronous early-onset LS tumors, with no family history of LS-associated cancers in their first-degree relatives. In one of the cases, the identified MLH1 constitutional methylation was monoallelic and results in MLH1 and EPM2AIP1 allele-specific transcriptional silencing. It was present in normal somatic tissues and absent in spermatozoa. The methylated MLH1 allele was maternally transmitted and methylation was reversed in a daughter who inherited the same allele. MLH1 methylation screening in lymphocyte DNA from patients with early-onset MLH1-methylated LS-associated tumors allows the identification of epimutation carriers. The present study adds further evidence to the emerging entity of soma-wide MLH1 epimutation and its heritability.
最近,在一部分林奇综合征(LS)病例中发现了 MLH1 外显子组的表观遗传突变。本研究的目的是在一组 34 例临床疑似 LS、MLH1 甲基化肿瘤和错配修复(MMR)基因未检测到种系突变的患者中,鉴定是否存在携带 MLH1 外显子组表观遗传突变的患者。采用 MS-MLPA(甲基化特异性多重连接依赖探针扩增)分析淋巴细胞 DNA 样本中的 MLH1 启动子甲基化。通过 MS-MCA(甲基化特异性熔解曲线分析)、亚硫酸氢盐测序和焦磷酸测序在不同的生物样本中对 MLH1 结构甲基化进行确认。使用杂合多态性确定等位基因表达。通过 MS-MLPA 和单倍型分析评估垂直传递。MS-MLPA 分析在 34 例结直肠癌 MLH1 甲基化的个体中有 2 例(5.9%)检测到 MLH1 结构甲基化。这些结果通过基于亚硫酸氢盐的方法得到了证实。两位外显子组突变携带者均发生了同时性早发性 LS 肿瘤,其一级亲属中无 LS 相关癌症的家族史。在一个病例中,鉴定出的 MLH1 结构甲基化为单等位基因,导致 MLH1 和 EPM2AIP1 等位基因特异性转录沉默。该突变存在于正常的体细胞组织中,不存在于精子中。携带甲基化 MLH1 等位基因的是母亲遗传,而在继承相同等位基因的女儿中,甲基化得到了逆转。在 MLH1 甲基化的 LS 相关早发性肿瘤患者的淋巴细胞 DNA 中进行 MLH1 甲基化筛选,可识别外显子组突变携带者。本研究进一步证实了广泛的 MLH1 外显子组表观遗传突变及其遗传性。