Suppr超能文献

16号染色体长臂标记与肾母细胞瘤家族易感性无连锁关系。

Nonlinkage of 16q markers to familial predisposition to Wilms' tumor.

作者信息

Huff V, Reeve A E, Leppert M, Strong L C, Douglass E C, Geiser C F, Li F P, Meadows A, Callen D F, Lenoir G

机构信息

Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030.

出版信息

Cancer Res. 1992 Nov 1;52(21):6117-20.

PMID:1356625
Abstract

Wilms' tumor (WT), a childhood cancer of the kidney, occurs in both familial and sporadic forms. Chromosome 11 genes have been implicated in the etiology of WT, and mutations in a gene at chromosomal band 11p13, WT1, have been identified in a few WT cases. However, 11p13 has been excluded as the site of the predisposition mutation segregating in several large WT families, which implies the existence of a non-11p familial predisposition gene. Recently, loss of heterozygosity for 16q markers located between chromosomal bands 16q13 and 16q22 has been reported in approximately 20% of sporadic Wilms' tumors. To determine if this region of 16q harbors the non-11p familial WT gene, a genetic linkage study of five WT families was undertaken. Using multipoint analyses, we ruled out genetic linkage of familial WT predisposition to 16q.

摘要

肾母细胞瘤(WT)是一种儿童期肾癌,有家族性和散发性两种形式。11号染色体上的基因与WT的病因有关,在少数WT病例中已鉴定出位于染色体带11p13的一个基因WT1发生了突变。然而,在几个大型WT家族中,11p13已被排除为分离的易感性突变位点,这意味着存在一个非11p的家族性易感基因。最近,据报道,在约20%的散发性肾母细胞瘤中,位于染色体带16q13和16q22之间的16q标记存在杂合性缺失。为了确定16q的这个区域是否含有非11p的家族性WT基因,对五个WT家族进行了基因连锁研究。通过多点分析,我们排除了家族性WT易感性与16q的基因连锁。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验