Cologne Center for Genomics (CCG), University of Cologne, Cologne, Germany.
Luxembourg Centre for Systems Biomedicine, University Luxembourg, Luxembourg, Luxembourg.
Eur J Hum Genet. 2019 Nov;27(11):1738-1744. doi: 10.1038/s41431-019-0484-4. Epub 2019 Jul 29.
It is challenging to estimate genetic variant burden across different subtypes of epilepsy. Herein, we used a comparative approach to assess the genetic variant burden and genotype-phenotype correlations in four most common brain lesions in patients with drug-resistant focal epilepsy. Targeted sequencing analysis was performed for a panel of 161 genes with a mean coverage of >400×. Lesional tissue was histopathologically reviewed and dissected from hippocampal sclerosis (n = 15), ganglioglioma (n = 16), dysembryoplastic neuroepithelial tumors (n = 8), and focal cortical dysplasia type II (n = 15). Peripheral blood (n = 12) or surgical tissue samples histopathologically classified as lesion-free (n = 42) were available for comparison. Variants were classified as pathogenic or likely pathogenic according to American College of Medical Genetics and Genomics guidelines. Overall, we identified pathogenic and likely pathogenic variants in 25.9% of patients with a mean coverage of 383×. The highest number of pathogenic/likely pathogenic variants was observed in patients with ganglioglioma (43.75%; all somatic) and dysembryoplastic neuroepithelial tumors (37.5%; all somatic), and in 20% of cases with focal cortical dysplasia type II (13.33% somatic, 6.67% germline). Pathogenic/likely pathogenic positive genes were disorder specific and BRAF V600E the only recurrent pathogenic variant. This study represents a reference for the genetic variant burden across the four most common lesion entities in patients with drug-resistant focal epilepsy. The observed large variability in variant burden by epileptic lesion type calls for whole exome sequencing of histopathologically well-characterized tissue in a diagnostic setting and in research to discover novel disease-associated genes.
评估不同类型癫痫的遗传变异负担具有挑战性。在此,我们采用比较方法评估了耐药性局灶性癫痫患者的四种最常见脑病变中遗传变异负担和基因型-表型相关性。对 161 个基因进行了靶向测序分析,平均覆盖率>400×。对海马硬化症(n=15)、神经节细胞瘤(n=16)、发育不良性神经上皮肿瘤(n=8)和局灶性皮质发育不良 II 型(n=15)的组织进行了组织病理学回顾和解剖。有外周血(n=12)或组织病理学分类为无病变的手术样本(n=42)可供比较。根据美国医学遗传学与基因组学学院的指南,将变异分类为致病性或可能致病性。总体而言,我们在 25.9%的患者中发现了致病性或可能致病性的变异,平均覆盖率为 383×。致病性/可能致病性变异数量最多的患者是神经节细胞瘤(43.75%;均为体细胞)和发育不良性神经上皮肿瘤(37.5%;均为体细胞),局灶性皮质发育不良 II 型患者中也有 20%(13.33%为体细胞,6.67%为种系)。致病性/可能致病性阳性基因是疾病特异性的,BRAF V600E 是唯一的复发性致病性变异。本研究代表了耐药性局灶性癫痫患者四种最常见病变实体的遗传变异负担参考。观察到的遗传变异负担在癫痫病变类型上的巨大差异需要在诊断环境中对组织病理学特征良好的组织进行全外显子组测序,并在研究中发现新的疾病相关基因。