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亚显微染色体易位中断点的检测,阐明了遗传疾病的一种重要机制。

Detection of breakpoints in submicroscopic chromosomal translocation, illustrating an important mechanism for genetic disease.

作者信息

Lamb J, Wilkie A O, Harris P C, Buckle V J, Lindenbaum R H, Barton N J, Reeders S T, Weatherall D J, Higgs D R

机构信息

Institute of Molecular Medicine, John Radcliffe Hospital, Oxford.

出版信息

Lancet. 1989 Oct 7;2(8667):819-24. doi: 10.1016/s0140-6736(89)92995-4.

Abstract

A 3-year-old boy presented with alpha-thalassaemia, dysmorphic features, and mental handicap. His younger sister is also mentally retarded, but haematologically normal. High resolution cytogenetic analysis revealed a normal karyotype in all family members. However, a combination of DNA analysis and in situ hybridisation demonstrated that the mother has a previously unsuspected balanced reciprocal translocation between the tips of the short arms of chromosomes 1 and 16, and that the alpha-globin gene complex (which maps to the tip of chromosome 16) is included in the translocated segment. Both of her children have inherited one of the translocation chromosomes in an unbalanced fashion: the boy has the derived chromosome 16, and therefore has alpha-thalassaemia, whilst the girl has the derived chromosome 1. Such cytogenetically invisible subtelomeric translocations are probably an important and hitherto unrecognised cause of genetic disease.

摘要

一名3岁男孩表现出α地中海贫血、畸形特征和智力障碍。他的妹妹也有智力发育迟缓,但血液学检查正常。高分辨率细胞遗传学分析显示所有家庭成员的核型均正常。然而,DNA分析和原位杂交相结合表明,母亲存在先前未被怀疑的1号和16号染色体短臂末端之间的平衡相互易位,并且α珠蛋白基因复合体(定位于16号染色体末端)包含在易位片段中。她的两个孩子都以不平衡的方式继承了其中一条易位染色体:男孩继承了衍生的16号染色体,因此患有α地中海贫血,而女孩继承了衍生的1号染色体。这种细胞遗传学上不可见的亚端粒易位可能是遗传疾病的一个重要且迄今未被认识的原因。

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