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在威尔姆斯瘤杂种中,人类T细胞急性淋巴细胞白血病中t(11;14)断点侧翼的11号染色体区域缺失。

The chromosome 11 region flanking the t(11;14) breakpoint in human T-ALL is deleted in Wilms' tumor hybrids.

作者信息

Finver S N, Martiniere C, Kagan J, Cavenee W, Croce C M

机构信息

Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

出版信息

Oncogene Res. 1989;5(2):143-8.

PMID:2558334
Abstract

Human chromosomal band 11p13 has been implicated in T cell malignancies carrying t(11;14)(p13;q11) reciprocal translocations and has also been associated with Wilms' tumor and aniridia in a mechanism characterized by overlapping hemizygous constitutional deletions spanning this region. Using probes derived from the T cell receptor delta gene, we have cloned the chromosomal breakpoint in an acute T cell leukemia (T-ALL). Southern blotting analyses of mouse-human somatic cell hybrids from this human T-ALL sample and Chinese hamster-human somatic cell hybrids derived from Wilms' tumor lines have indicated that the 11p13 locus, tcl-2, juxtaposed to the TCR (T cell receptor) delta locus in T cell leukemia, is within the constitutional deletion of two Wilms' tumor-aniridia cases.

摘要

人类染色体带11p13与携带t(11;14)(p13;q11)相互易位的T细胞恶性肿瘤有关,并且还与威尔姆斯瘤和无虹膜症相关,其机制的特征是跨越该区域的半合子性结构缺失重叠。利用源自T细胞受体δ基因的探针,我们克隆了一例急性T细胞白血病(T-ALL)中的染色体断点。对来自该人类T-ALL样本的小鼠-人类体细胞杂种以及源自威尔姆斯瘤细胞系的中国仓鼠-人类体细胞杂种进行的Southern印迹分析表明,在T细胞白血病中与TCR(T细胞受体)δ基因座并列的11p13位点tcl-2,位于两例威尔姆斯瘤-无虹膜症病例的结构缺失范围内。

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