Association of TMPRSS2-ERG gene fusion with clinical characteristics and outcomes: results from a population-based study of prostate cancer.
Association of TMPRSS2-ERG gene fusion with clinical characteristics and outcomes: results from a population-based study of prostate cancer.
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TMPRSS2-ERG 基因融合与临床特征和结果的关联：基于人群的前列腺癌研究的结果。
DOI：
10.1186/1471-2407-8-230
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发表时间：
2008-08-11
期刊：
影响因子：
3.8
通讯作者：
Huntsman, David G.
中科院分区：
文献类型：
--
作者：
FitzGerald, Liesel M.;Agalliu, Ilir;Johnson, Karynn;Miller, Melinda A.;Kwon, Erika M.;Hurtado-Coll, Antonio;Fazli, Ladan;Rajput, Ashish B.;Gleave, Martin E.;Cox, Michael E.;Ostrander, Elaine A.;Stanford, Janet L.;Huntsman, David G.
TMPRSS2-ERG融合基因在前列腺癌中的存在最近被认为与前列腺癌的侵袭性表型以及复发和死亡有关。这些关联表明，基因融合可以作为前列腺癌的预后指标的假设。在这项研究中，荧光原位杂交(FISH)分析了来自两个人群研究的214例前列腺癌患者的TMPRSS2-ERG融合状态。FISH分析被设计用来检测融合类型(缺失与易位)和融合拷贝数(单一与多个)。其中一个病例(n=127)的4个ERG和1个TMPRSS2 SNPs用胚系DNA进行了基因分型。在TMPRSS2-ERG融合评分的214个肿瘤中，64.5%为阴性，35.5%为阳性。TMPRSS2-ERG融合患者的前列腺癌生存率没有下降(HR=0.92，95%CI=0.22-3.93)，按易位或缺失(HR=0.84，95%CI=0.23-3.12)或保留融合拷贝数(HR=1.22，95%CI=0.45-3.34)分层后，前列腺癌的特定原因生存率也没有显著差异。然而，在那些肿瘤具有多个融合副本的病例中，前列腺癌特异性存活率降低的证据是显而易见的。TMPRSS2SNP变异T等位基因rs12329760通过易位与TMPRSS2-ERG融合呈正相关(p=0.05)，与多拷贝基因融合呈正相关(p=0.03)。如果重复，本文提出的结果可能为TMPRSS2-ERG基因融合的发生机制提供洞察，并有助于诊断评估，以确定将继续发展为转移性前列腺癌的男性亚群。
The presence of the TMPRSS2-ERG fusion gene in prostate tumors has recently been associated with an aggressive phenotype, as well as recurrence and death from prostate cancer. These associations suggest the hypothesis that the gene fusion may be used as a prognostic indicator for prostate cancer. In this study, fluorescent in situ hybridization (FISH) assays were used to assess TMPRSS2-ERG fusion status in a group of 214 prostate cancer cases from two population-based studies. The FISH assays were designed to detect both fusion type (deletion vs. translocation) and the number of fusion copies (single vs. multiple). Genotyping of four ERG and one TMPRSS2 SNPs using germline DNA was also performed in a sample of the cases (n = 127). Of the 214 tumors scored for the TMPRSS2-ERG fusion, 64.5% were negative and 35.5% were positive for the fusion. Cases with the TMPRSS2-ERG fusion did not exhibit reduced prostate cancer survival (HR = 0.92, 95% CI = 0.22–3.93), nor was there a significant difference in cause-specific survival when stratifying by translocation or deletion (HR = 0.84, 95% CI = 0.23–3.12) or by the number of retained fusion copies (HR = 1.22, 95% CI = 0.45–3.34). However, evidence for reduced prostate cancer-specific survival was apparent in those cases whose tumor had multiple copies of the fusion. The variant T allele of the TMPRSS2 SNP, rs12329760, was positively associated with TMPRSS2-ERG fusion by translocation (p = 0.05) and with multiple copies of the gene fusion (p = 0.03). If replicated, the results presented here may provide insight into the mechanism by which the TMPRSS2-ERG gene fusion arises and also contribute to diagnostic evaluations for determining the subset of men who will go on to develop metastatic prostate cancer.
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