Bertola Débora R, Yamamoto Guilherme L, Almeida Tatiana F, Buscarilli Michelle, Jorge Alexander A L, Malaquias Alexsandra C, Kim Chong A, Takahashi Vanessa N V, Passos-Bueno Maria Rita, Pereira Alexandre C
Unidade de Genética do Instituto da Criança, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/SP, Brazil; Instituto de Biociências, Universidade de São Paulo, São Paulo/SP, Brazil.
Am J Med Genet A. 2014 Nov;164A(11):2952-7. doi: 10.1002/ajmg.a.36722. Epub 2014 Aug 13.
Noonan syndrome (NS) is an autosomal dominant disorder consisting of short stature, short and/or webbed neck, distinctive facial features, cardiac abnormalities, cryptorchidism, and coagulation defects. NS exhibits genetic heterogeneity, associated with mutated genes that participate in RAS-mitogen-activated protein kinase signal transduction. Recently, a new gene (RIT1) was discovered as the causative gene in 17 of 180 Japanese individuals who were negative for the previously known genes for NS and were studied using exome sequencing (four patients), followed by Sanger sequencing (13 patients). The present study used the same technique in 70 Brazilian patients with NS and identified six with RIT1 missense mutations. Thus, we confirm that RIT1 is responsible for approximately 10% of the patients negative for mutations in the previously known genes. The phenotype includes a high frequency of high birth weight, relative macrocephaly, left ventricular hypertrophy, and ectodermal findings, such as curly hair, hyperpigmentation, and wrinkled palms and soles. Short stature and pectus deformity were less frequent. The majority of patients with a RIT1 mutation did not show apparent intellectual disability. Because of the relatively high frequency of mutations in RIT1 among patients with NS and its occurrence in different populations, we suggest that it should be added to the list of genes included in panels for the molecular diagnosis of NS through targeted next-generation sequencing.
努南综合征(NS)是一种常染色体显性疾病,其特征包括身材矮小、颈部短和/或有蹼、独特的面部特征、心脏异常、隐睾症和凝血缺陷。NS表现出遗传异质性,与参与RAS-丝裂原活化蛋白激酶信号转导的突变基因相关。最近,在180名对先前已知的NS基因检测呈阴性的日本个体中,通过外显子组测序(4例患者),随后进行桑格测序(13例患者),发现了一个新基因(RIT1)是致病基因。本研究对70名巴西NS患者采用了相同技术,鉴定出6例有RIT1错义突变。因此,我们证实RIT1导致了约10%先前已知基因无突变的患者发病。其表型包括高出生体重、相对巨头畸形、左心室肥厚以及外胚层表现,如卷发、色素沉着过度、手掌和足底有皱纹等的高发生率。身材矮小和漏斗胸畸形的发生率较低。大多数RIT1突变患者未表现出明显的智力残疾。由于NS患者中RIT1突变的频率相对较高且在不同人群中均有发生,我们建议应将其添加到通过靶向新一代测序进行NS分子诊断的基因检测面板所包含的基因列表中。