Garcia-Heras J, Martin J A, Witchel S F, Scacheri P
Genetic Testing Center, Texas Department of Health, Denton 76202-2467, USA.
J Med Genet. 1997 Mar;34(3):242-5. doi: 10.1136/jmg.34.3.242.
We describe an 11 year old girl with a de novo unbalanced t(X;10) that resulted in a deletion of Xq26-->Xqter and a trisomy of 10q21-->10qter. Her clinical features were of distal trisomy 10q, but she lacked the cardiovascular and renal malformations observed in duplications of 10q24-->10qter and had only moderate mental retardation. X inactivation was assessed on peripheral blood lymphocytes by late replication with BrdU (LR) and the human androgen receptor assay (HAR). By LR the der(X) was inactive without spreading to 10q21-->10qter in all cells. The HAR assay showed skewed methylation of the paternal allele (90%). The correlation of HAR and LR suggests that the der(X) was paternally inherited and is consistent with data from other de novo balanced and unbalanced X;autosome translocations detected in females. This is the first report of parental origin of a de novo trisomy 10q.
我们描述了一名11岁女孩,其存在一条从头发生的不平衡t(X;10),导致Xq26至Xqter缺失以及10q21至10qter三体。她的临床特征为10q远端三体,但她没有10q24至10qter重复中观察到的心血管和肾脏畸形,仅有中度智力发育迟缓。通过用溴脱氧尿苷(BrdU)进行晚期复制(LR)和人雄激素受体检测(HAR)对外周血淋巴细胞进行X染色体失活评估。通过LR,在所有细胞中,衍生X染色体(der(X))均无活性,且未扩展至10q21至10qter。HAR检测显示父本等位基因甲基化偏斜(90%)。HAR和LR的相关性表明der(X)是父本遗传的,这与在女性中检测到的其他从头发生的平衡和不平衡X;常染色体易位的数据一致。这是关于从头发生的10q三体的亲本来源的首次报告。