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本文引用的文献

1
Therapeutic targeting of SPINK1-positive prostate cancer.靶向 SPINK1 阳性前列腺癌的治疗。
Sci Transl Med. 2011 Mar 2;3(72):72ra17. doi: 10.1126/scitranslmed.3001498.
2
The genomic complexity of primary human prostate cancer.原发性人类前列腺癌的基因组复杂性。
Nature. 2011 Feb 10;470(7333):214-20. doi: 10.1038/nature09744.
3
Triggers for genomic rearrangements: insights into genomic, cellular and environmental influences.基因组重排的触发因素:对基因组、细胞和环境影响的深入了解。
Nat Rev Genet. 2010 Dec;11(12):819-29. doi: 10.1038/nrg2883. Epub 2010 Nov 3.
4
Androgen-induced TMPRSS2:ERG fusion in nonmalignant prostate epithelial cells.雄激素诱导的非恶性前列腺上皮细胞中的 TMPRSS2:ERG 融合。
Cancer Res. 2010 Dec 1;70(23):9544-8. doi: 10.1158/0008-5472.CAN-10-1638. Epub 2010 Oct 14.
5
Antibody-based detection of ERG rearrangement-positive prostate cancer.基于抗体的 ERG 重排阳性前列腺癌检测。
Neoplasia. 2010 Jul;12(7):590-8. doi: 10.1593/neo.10726.
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Cancer statistics, 2010.癌症统计数据,2010 年。
CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300. doi: 10.3322/caac.20073. Epub 2010 Jul 7.
7
Androgen-induced TOP2B-mediated double-strand breaks and prostate cancer gene rearrangements.雄激素诱导的 TOP2B 介导的双链断裂和前列腺癌基因重排。
Nat Genet. 2010 Aug;42(8):668-75. doi: 10.1038/ng.613. Epub 2010 Jul 4.
8
Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma.前列腺癌、胃癌和黑色素瘤中 RAF 激酶通路的重排。
Nat Med. 2010 Jul;16(7):793-8. doi: 10.1038/nm.2166. Epub 2010 Jun 6.
9
Prevalence of TMPRSS2-ERG and SLC45A3-ERG gene fusions in a large prostatectomy cohort.在一个大型前列腺切除术队列中 TMPRSS2-ERG 和 SLC45A3-ERG 基因融合的流行率。
Mod Pathol. 2010 Apr;23(4):539-46. doi: 10.1038/modpathol.2009.193. Epub 2010 Jan 29.
10
Nuclear receptor-induced chromosomal proximity and DNA breaks underlie specific translocations in cancer.核受体诱导的染色体接近和 DNA 断裂是癌症中特定易位的基础。
Cell. 2009 Dec 11;139(6):1069-83. doi: 10.1016/j.cell.2009.11.030.

前列腺癌的常见基因重排。

Common gene rearrangements in prostate cancer.

机构信息

Weill Cornell Medical College, 1300 York Ave, Room C 410-A, New York, NY 10021, USA.

出版信息

J Clin Oncol. 2011 Sep 20;29(27):3659-68. doi: 10.1200/JCO.2011.35.1916. Epub 2011 Aug 22.

DOI:10.1200/JCO.2011.35.1916
PMID:21859993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4874145/
Abstract

Prostate cancer is a common heterogeneous disease, and most patients diagnosed in the post prostate-specific antigen (PSA) era present with clinically localized disease, the majority of which do well regardless of treatment regimen undertaken. Overall, those with advanced prostate cancer at time of diagnosis do poorly after androgen withdrawal therapy. Understanding the biologic underpinning of prostate cancer is necessary to best determine the risk of disease progression and would be advantageous for the development of novel therapeutic approaches to impede or prevent disease. This review focuses on the recently identified common ETS and non-ETS gene rearrangements in prostate cancer. Although multiple molecular alterations have been detected in prostate cancer, a detailed understanding of gene fusion prostate cancer should help explain the clinical and biologic diversity, providing a rationale for a molecular subclassification of the disease.

摘要

前列腺癌是一种常见的异质性疾病,大多数在前列腺特异性抗原(PSA)时代后被诊断出患有局限性疾病的患者,无论采用何种治疗方案,大多数患者预后良好。总体而言,在雄激素剥夺治疗时被诊断为晚期前列腺癌的患者预后较差。了解前列腺癌的生物学基础对于最佳确定疾病进展的风险是必要的,并且有利于开发新的治疗方法来阻碍或预防疾病。这篇综述重点介绍了最近在前列腺癌中发现的常见 ETS 和非 ETS 基因重排。尽管在前列腺癌中已经检测到多种分子改变,但对基因融合前列腺癌的详细了解应该有助于解释临床和生物学多样性,为疾病的分子分类提供依据。