Wilson G N, Dasouki M, Barr M
Department of Medical Genetics, McGill University, Montreal, Quebec, Canada.
Am J Med Genet Suppl. 1986;2:65-72. doi: 10.1002/ajmg.1320250610.
Four cases of holoprosencephaly with duplication/deletion involving chromosome 13 are presented and additional cases are summarized from the literature. When examined as a series, the duplications (trisomy 13, trisomy 13pter----q14) and deletions (deletion 13q12----qter, deletion 13q31----qter, ring 13 with deletion 13q14----qter) exclude deletion or duplication of single chromosome 13 bands as the cause for holoprosencephaly. Increased dosage of the 13pter----q14 region relative to the 13q14----qter region as the cause is also ruled out by the duplication 13q21----qter cases reported in the literature. Altered timing of forebrain development, causing reversion to a more primitive embryonic and phylogenetic brain structure, is related to dosage imbalance of at least two chromosome 13 regions.
本文报告了4例伴有13号染色体重复/缺失的前脑无裂畸形病例,并从文献中总结了其他病例。将这些病例作为一个系列进行研究时,重复(13三体、13pter→q14三体)和缺失(13q12→qter缺失、13q31→qter缺失、伴有13q14→qter缺失的13号环状染色体)排除了单个13号染色体带的缺失或重复作为前脑无裂畸形病因的可能性。文献中报道的13q21→qter重复病例也排除了相对于13q14→qter区域而言13pter→q14区域剂量增加作为病因的可能性。前脑发育时间改变导致向更原始的胚胎和系统发育脑结构逆转,这与至少两个13号染色体区域的剂量失衡有关。