Taliercio V, Zhao J, Boyden S E, Mao R, Bayrak-Toydemir P, Pflaum A, Palumbos J, Andrews A, Baldwin E E, Welt C, Fait Mackenzie, Botto L D, Viskochil D
Department of Pediatrics, Division of Medical Genetics, University of Utah, Salt Lake City, Utah, USA.
Department of Pathology, University of Utah, Salt Lake City, Utah, USA.
Am J Med Genet A. 2025 Sep;197(9):e64108. doi: 10.1002/ajmg.a.64108. Epub 2025 May 3.
Gorlin-Goltz Syndrome (GGS) is a rare autosomal dominant genetic disorder encompassing a diverse range of clinical manifestations, including congenital anomalies and predisposition to cancer. Pathogenic variants in PTCH1 and SUFU account for up to 79% and 6% of cases, respectively. Currently, an estimated 15%-27% of individuals with a clinical diagnosis of GGS do not have a pathogenic variant identified in either gene. We report on a 17-year-old female referred to the Undiagnosed Disease Network with a clinical diagnosis of GGS that manifested as both classic and unusual findings, including isolated hypogonadotropic hypogonadism and anosmia (Kallmann syndrome), orofacial cleft, and abnormal semicircular canals (SCC). Prior genetic testing, including a targeted gene panel, genomic microarray, exome sequencing, and genome sequencing, was non-diagnostic, although these studies identified a variant of uncertain significance in CHD7, which may have contributed to elements of the phenotype (e.g., abnormal SCC). Reanalysis of genome sequencing data using research analytic methods, together with karyotyping, FISH, and Sanger sequencing, identified a novel de novo paracentric inversion that truncated PTCH1. These findings underscore the value of in-depth phenotype-guided genomic analysis, including chromosomal structural variants, as well as the occurrence of possible dual genetic diagnoses in the same individuals. Moreover, the definitive diagnosis provided the patient and family with a firmer basis for management and counseling.
戈林-戈尔茨综合征(GGS)是一种罕见的常染色体显性遗传病,临床表现多样,包括先天性异常和易患癌症。PTCH1和SUFU的致病变异分别占病例的79%和6%。目前,临床诊断为GGS的患者中,估计有15%-27%在这两个基因中均未发现致病变异。我们报告了一名17岁女性,因临床诊断为GGS被转诊至未确诊疾病网络,其表现既有典型症状也有不寻常症状,包括孤立性低促性腺激素性性腺功能减退和嗅觉缺失(卡尔曼综合征)、口面部裂隙以及异常的半规管(SCC)。尽管之前的基因检测,包括靶向基因panel、基因组微阵列、外显子组测序和基因组测序均未得出诊断结果,但这些研究在CHD7中发现了一个意义未明的变异,该变异可能导致了部分表型(如异常的SCC)。使用研究分析方法对基因组测序数据进行重新分析,结合核型分析、荧光原位杂交(FISH)和桑格测序,发现了一种新的从头发生的臂间倒位,该倒位截断了PTCH1。这些发现强调了深入的表型引导的基因组分析(包括染色体结构变异)的价值,以及同一个体可能出现双重基因诊断的情况。此外,明确的诊断为患者及其家庭提供了更坚实的管理和咨询基础。