Ferrarini Alessandra, Gaillard Muriel, Guerry Frederic, Ramelli Gianpaolo, Heidi Fodstad, Keddache Caroline Verley, Wieland Ilse, Beckmann Jacques S, Jaquemont Sébastien, Martinet Danielle
Division of Pediatrics, San Giovanni Hospital, Bellinzona, Switzerland.
Am J Med Genet A. 2014 Feb;164A(2):346-52. doi: 10.1002/ajmg.a.36140. Epub 2013 Dec 13.
Frontonasal dysplasia (FND) is a genetically heterogeneous malformation spectrum with marked hypertelorism, broad nasal tip and bifid nose. Only a small number of genes have been associated with FND phenotypes until now, the first gene being EFNB1, related to craniofrontonasal syndrome (CFNS) with craniosynostosis in addition, and more recently the aristaless-like homeobox genes ALX3, ALX4, and ALX1, which have been related with distinct phenotypes named FND1, FND2, and FND3 respectively. We here report on a female patient presenting with severe FND features along with partial alopecia, hypogonadism and intellectual disability. While molecular investigations did not reveal mutations in any of the known genes, ALX4, ALX3, ALX1 and EFNB1, comparative genomic hybridization (array CGH) techniques showed a large heterozygous de novo deletion at 11p11.12p12, encompassing the ALX4 gene. Deletions in this region have been described in patients with Potocki-Shaffer syndrome (PSS), characterized by biparietal foramina, multiple exostoses, and intellectual disability. Although the patient reported herein manifests some overlapping features of FND and PPS, it is likely that the observed phenotype maybe due to a second unidentified mutation in the ALX4 gene. The phenotype will be discussed in view of the deleted region encompassing the ALX4 gene.
额鼻发育异常(FND)是一种具有明显眼距过宽、鼻尖宽阔和鼻裂的基因异质性畸形谱。到目前为止,只有少数基因与FND表型相关,第一个基因是EFNB1,此外还与伴有颅缝早闭的颅额鼻综合征(CFNS)相关,最近还有无触角样同源盒基因ALX3、ALX4和ALX1,它们分别与名为FND1、FND2和FND3的不同表型相关。我们在此报告一名女性患者,其具有严重的FND特征,同时伴有部分脱发、性腺功能减退和智力残疾。虽然分子研究未在任何已知基因ALX4、ALX3、ALX1和EFNB1中发现突变,但比较基因组杂交(阵列CGH)技术显示在11p11.12p12处有一个大的杂合性新发缺失,包含ALX4基因。该区域的缺失已在波托基-谢弗综合征(PSS)患者中被描述,其特征为双侧顶骨孔、多发性骨疣和智力残疾。尽管本文报道的患者表现出一些FND和PPS的重叠特征,但观察到的表型可能是由于ALX4基因中另一个未鉴定的突变所致。将根据包含ALX4基因的缺失区域来讨论该表型。