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人类前列腺癌中BRCA1及17号染色体长臂上其他基因座的杂合性缺失

Loss of heterozygosity of the BRCA1 and other loci on chromosome 17q in human prostate cancer.

作者信息

Gao X, Zacharek A, Salkowski A, Grignon D J, Sakr W, Porter A T, Honn K V

机构信息

Department of Radiation Oncology (Cancer Biology Division), Wayne State University School of Medicine, Detroit, Michigan 48202.

出版信息

Cancer Res. 1995 Mar 1;55(5):1002-5.

PMID:7866981
Abstract

A putative tumor suppressor gene, the BRCA1 gene, on chromosome 17q21 has recently been identified and shown to be mutated in breast and ovarian cancers. We have undertaken the present study to explore the possible involvement of the BRCA1 and/or other potential genes on chromosome 17q in prostate cancer. Twenty-three patients were screened by PCR for loss of heterozygosity at five microsatellite loci spanning the region of 17q12-21. One of the loci (i.e., D17S855) studied is intragenic to the BRCA1. Forty-four and 40% of the informative cases showed loss of heterozygosity at the BRCA1 (D17S855) and D17S856 loci, respectively, whereas 10%, 10%, and 11% of the informative cases were positive for loss of heterozygosity at the D17S250, D17S579, and D17S588 loci, respectively. Overall, 52% (11/21) of the informative cases have allelic loss of at least one locus on chromosome 17q. Our data suggest that the BRCA1 and/or other genes within the interval between BRCA1 and D17S856 on 17q21 may be important in the pathogenesis of prostate cancer.

摘要

一个假定的肿瘤抑制基因,即位于17号染色体q21区域的BRCA1基因,最近已被鉴定出来,并显示在乳腺癌和卵巢癌中发生了突变。我们开展了本研究,以探索17号染色体q上的BRCA1和/或其他潜在基因在前列腺癌中的可能作用。通过聚合酶链反应(PCR)对23例患者进行检测,以确定跨越17q12 - 21区域的5个微卫星位点的杂合性缺失情况。所研究的其中一个位点(即D17S855)位于BRCA1基因内部。在有信息价值的病例中,分别有44%和40%在BRCA1(D17S855)和D17S856位点显示杂合性缺失,而在有信息价值的病例中,分别有10%、10%和11%在D17S250、D17S579和D17S588位点杂合性缺失呈阳性。总体而言,52%(11/21)有信息价值的病例在17号染色体q上至少有一个位点出现等位基因缺失。我们的数据表明,BRCA1和/或17q21上BRCA1与D17S856之间区域内的其他基因可能在前列腺癌的发病机制中起重要作用。

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Loss of heterozygosity of the BRCA1 and other loci on chromosome 17q in human prostate cancer.人类前列腺癌中BRCA1及17号染色体长臂上其他基因座的杂合性缺失
Cancer Res. 1995 Mar 1;55(5):1002-5.
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