Schulz Solveig, Volleth Marianne, Muschke Petra, Wieland Ilse, Wieacker Peter
Institute of Human Genetics, Otto-von-Guericke University Magdeburg, Germany.
Appl Clin Genet. 2008 Nov 18;1:19-22. doi: 10.2147/tacg.s4401. Print 2008.
We report on a six years old boy with several features of Greig cephalopolysyndactyly syndrome (GCPS) including craniofacial dysmorphism, hypertelorism, heart defect, preaxial hexadactyly of toes, partial agenesis of corpus callosum, and severe developmental delay. Greig cephalopolysyndactyly (GCPS) can be caused by GLI3 deletions. In patients with large deletions which include additional genes, it is termed Greig cephalopolysyndactyly-contiguous gene syndrome (GCPS-CGS). It is generally believed that the deletion size correlates with disease severity. Nearly all cases appear to be a result of GLI3 de novo deletions. Chromosome analysis of our patient revealed a large deletion in chromosome 7(p13-p14). Unlike most previously described cases, we found that this deletion resulted from a paternal balanced insertional translocation of 7p13-14 into the long arm of chromosome 5.
我们报告了一名6岁男孩,他具有格雷格头多指综合征(GCPS)的多种特征,包括颅面畸形、眼距过宽、心脏缺陷、脚趾轴前多指畸形、胼胝体部分发育不全以及严重发育迟缓。格雷格头多指综合征(GCPS)可由GLI3基因缺失引起。在存在包括其他基因的大片段缺失的患者中,称为格雷格头多指连续基因综合征(GCPS-CGS)。一般认为缺失大小与疾病严重程度相关。几乎所有病例似乎都是GLI3基因新发缺失的结果。对我们患者的染色体分析显示7号染色体(p13-p14)存在大片段缺失。与大多数先前描述的病例不同,我们发现这种缺失是由于父亲的7号染色体p13-14平衡插入易位到5号染色体长臂所致。