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通过比较基因组杂交显示的日本患者局限性前列腺癌的基因变化。

Genetic changes in localized prostate cancer of Japanese patients shown by comparative genomic hybridization.

作者信息

Kasahara Kotaro, Taguchi Takahiro, Yamasaki Ichiro, Kamada Masayuki, Shuin Taro

机构信息

Department of Urology, Kochi Medical School, Nankoku, Kochi, Japan.

出版信息

Cancer Genet Cytogenet. 2005 May;159(1):84-8. doi: 10.1016/j.cancergencyto.2004.09.006.

Abstract

To search for additional amplification and deletion sites that may serve as a starting point for the discovery of new oncogenes or tumor suppressor genes, 30 Japanese localized prostate cancers were analyzed by comparative genomic hybridization (CGH) in this study. CGH was used to search for changes in DNA sequence copy-number in a series of 30 primary prostate adenocarcinomas, consisting of 22 cases of pT2N0 (organ confined; without capsular invasion) and 8 cases of pT3N0 (with capsular invasion), removed by radical prostatectomy. CGH revealed that the shortest regions of overlap (SRO) of gains in pT2N0 were at 8q22.2 approximately q24.2, 11q13.1 approximately q14.1, and 12q23 approximately q24.2, whereas the SRO of losses were seen at 8p23.3 approximately p22, 13q21.2 approximately p22, and 18q21 approximately q22. The SRO of gains in pT3N0 were noted at 5q32 approximately q34, 8q22.3 approximately q24.1, 11q14.1 approximately q22.3, and 12q22 approximately q24.2, whereas the SRO of losses were seen at 18q21.2 approximately q23. These results suggest that gains or losses of DNA in these regions are important for prostate cancer progression. The detection of the SRO may serve as a starting point to discover novel oncogenes and tumor suppressor genes involved in prostate cancer progression.

摘要

为了寻找可能作为发现新的癌基因或肿瘤抑制基因起点的额外扩增和缺失位点,本研究通过比较基因组杂交(CGH)分析了30例日本局限性前列腺癌。CGH用于搜索一系列30例原发性前列腺腺癌的DNA序列拷贝数变化,这些腺癌包括22例pT2N0(器官局限;无包膜侵犯)和8例pT3N0(有包膜侵犯),均通过根治性前列腺切除术切除。CGH显示,pT2N0中增益的最短重叠区域(SRO)位于8q22.2至约q24.2、11q13.1至约q14.1以及12q23至约q24.2,而缺失的SRO出现在8p23.3至约p22、13q21.2至约p22以及18q21至约q22。pT3N0中增益的SRO位于5q32至约q34、8q22.3至约q24.1、11q14.1至约q22.3以及12q22至约q24.2,而缺失的SRO出现在18q21.2至约q23。这些结果表明,这些区域DNA的增益或缺失对前列腺癌进展很重要。检测SRO可能作为发现参与前列腺癌进展的新型癌基因和肿瘤抑制基因的起点。

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