Institut für Humangenetik, Universitätsklinikum Essen, Universität Duisburg-Essen, Essen, Germany.
Department of Internal Medicine, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA.
Clin Genet. 2021 Aug;100(2):187-200. doi: 10.1111/cge.13977. Epub 2021 May 14.
Mutations affecting the transcriptional regulator Ankyrin Repeat Domain 11 (ANKRD11) are mainly associated with the multisystem developmental disorder known as KBG syndrome, but have also been identified in individuals with Cornelia de Lange syndrome (CdLS) and other developmental disorders caused by variants affecting different chromatin regulators. The extensive functional overlap of these proteins results in shared phenotypical features, which complicate the assessment of the clinical diagnosis. Additionally, re-evaluation of individuals at a later age occasionally reveals that the initial phenotype has evolved toward clinical features more reminiscent of a developmental disorder different from the one that was initially diagnosed. For this reason, variants in ANKRD11 can be ascribed to a broader class of disorders that fall within the category of the so-called chromatinopathies. In this work, we report on the clinical characterization of 23 individuals with variants in ANKRD11. The subjects present primarily with developmental delay, intellectual disability and dysmorphic features, and all but two received an initial clinical diagnosis of either KBG syndrome or CdLS. The number and the severity of the clinical signs are overlapping but variable and result in a broad spectrum of phenotypes, which could be partially accounted for by the presence of additional molecular diagnoses and distinct pathogenic mechanisms.
影响转录调节剂 ankrd11 基因突变主要与多系统发育障碍有关,称为 kbg 综合征,但也在 cornelia de lange 综合征(cdls)和其他由影响不同染色质调节剂的变异引起的发育障碍患者中发现。这些蛋白质的广泛功能重叠导致了共同的表型特征,这使得临床诊断的评估变得复杂。此外,在以后的年龄重新评估个体时,偶尔会发现最初的表型已经向更类似于最初诊断的发育障碍的临床特征演变。因此,ankrd11 中的变异可以归因于更广泛的一类疾病,这些疾病属于所谓的染色质病类别。在这项工作中,我们报告了 23 名 ankrd11 变异患者的临床特征。这些患者主要表现为发育迟缓、智力残疾和发育不良特征,除了两个以外,所有人都接受了 kbg 综合征或 cdls 的初始临床诊断。临床体征的数量和严重程度是重叠的,但也是可变的,导致了广泛的表型,这部分可以通过存在其他分子诊断和不同的发病机制来解释。