Department of Human Genetics, University Medicine Greifswald, and Interfaculty Institute of Genetics and Functional Genomics, University of Greifswald, Greifswald, Germany.
Institute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany.
Sci Rep. 2020 Apr 14;10(1):6306. doi: 10.1038/s41598-020-63337-5.
Autosomal dominant cerebral cavernous malformations (CCM) are leaky vascular lesions that can cause epileptic seizures and stroke-like symptoms. Germline mutations in either CCM1, CCM2 or CCM3 are found in the majority of patients with multiple CCMs or a positive family history. Recently, the first copy number neutral inversion in CCM2 has been identified by whole genome sequencing in an apparently mutation-negative CCM family. We here asked the question whether further structural genomic rearrangements can be detected within NGS gene panel data of unsolved CCM cases. Hybrid capture NGS data of eight index patients without a pathogenic single nucleotide, indel or copy number variant were analyzed using two bioinformatics pipelines. In a 58-year-old male with multiple CCMs in his brain and spinal cord, we identified a 294 kb insertion within the coding sequence of CCM2. Fine mapping of the breakpoints, molecular cytogenetic studies, and multiplex ligation-dependent probe amplification verified that the structural variation was an inverted unbalanced insertion that originated from 1p12-p11.2. As this rearrangement disrupts exon 6 of CCM2 on 7p13, it was classified as pathogenic. Our study demonstrates that efforts to detect structural variations in known disease genes increase the diagnostic sensitivity of genetic analyses for well-defined Mendelian disorders.
常染色体显性脑型海绵状血管畸形(CCM)是一种渗漏性血管病变,可引起癫痫发作和类似中风的症状。大多数多发性 CCM 或阳性家族史患者的 CCM1、CCM2 或 CCM3 种系突变。最近,通过全基因组测序在一个明显无突变的 CCM 家族中首次发现 CCM2 中的第一个拷贝数中性反转。我们在这里询问了一个问题,即在未解决的 CCM 病例的 NGS 基因面板数据中是否可以检测到其他结构性基因组重排。使用两种生物信息学管道分析了 8 名无致病单核苷酸、插入或缺失或拷贝数变异的索引患者的杂交捕获 NGS 数据。在一名 58 岁的男性中,他的大脑和脊髓中有多个 CCM,我们在 CCM2 的编码序列中发现了一个 294kb 的插入。断点的精细作图、分子细胞遗传学研究和多重连接依赖性探针扩增证实,该结构变异是一种源自 1p12-p11.2 的反转不平衡插入。由于该重排破坏了 7p13 上的 CCM2 外显子 6,因此将其归类为致病性。我们的研究表明,努力检测已知疾病基因中的结构变异可提高遗传分析对明确孟德尔疾病的诊断敏感性。