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通过荧光原位杂交以及载脂蛋白A-II、凝血因子V和抗凝血酶III的基因剂量分析鉴定出的1号染色体间质缺失[del(1)(q24q25.3)]

Interstitial deletion of chromosome 1q [del(1)(q24q25.3)] identified by fluorescence in situ hybridization and gene dosage analysis of apolipoprotein A-II, coagulation factor V, and antithrombin III.

作者信息

Takano T, Yamanouchi Y, Mori Y, Kudo S, Nakayama T, Sugiura M, Hashira S, Abe T

机构信息

Department of Hygiene and Public Health, Teikyo University School of Medicine, Tokyo, Japan.

出版信息

Am J Med Genet. 1997 Jan 20;68(2):207-10.

PMID:9028459
Abstract

We report on a 12-month-old Japanese boy with an interstitial deletion of the long-arm of chromosome 1 and meningomyelocele, hydrocephalus, anal atresia, atrial septal defect, left renal agenesis, bilateral cryptorchidism, talipes equinovarus, low birth weight, growth/developmental retardation, and many minor anomalies. By conventional GTG-banding, his karyotype was first interpreted as 46,XY,del(1)(q23q24), but it was corrected as 46,XY.ish del(1)(q24q25.3) by fluorescence in situ hybridization using 11 known cosmid clones as probes. His serum levels of apolipoprotein A-II (gene symbol: APOA2, previously assigned to 1q21-q23) and coagulation factor V (F5, 1q21-q25) were normal, while serum concentration and activity of antithrombin III (AT3, 1q23-q25.1) was low. The results indicated that localization of APOA2 and F5 are proximal to the deleted region and AT3 is located within the deletion extent in the patient.

摘要

我们报告了一名12个月大的日本男孩,他患有1号染色体长臂间质性缺失,并伴有脊髓脊膜膨出、脑积水、肛门闭锁、房间隔缺损、左肾缺如、双侧隐睾、马蹄内翻足、低出生体重、生长/发育迟缓以及许多轻微异常。通过传统的GTG显带技术,他的核型最初被解释为46,XY,del(1)(q23q24),但使用11个已知的黏粒克隆作为探针进行荧光原位杂交后,被校正为46,XY.ish del(1)(q24q25.3)。他的血清载脂蛋白A-II(基因符号:APOA2,先前定位于1q21-q23)和凝血因子V(F5,1q21-q25)水平正常,而抗凝血酶III(AT3,1q23-q25.1)的血清浓度和活性较低。结果表明,APOA2和F5的定位在缺失区域近端,而AT3位于患者的缺失范围内。

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