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本文引用的文献

1
Identification of a cell of origin for human prostate cancer.鉴定人类前列腺癌的起源细胞。
Science. 2010 Jul 30;329(5991):568-71. doi: 10.1126/science.1189992.
2
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.
3
NKX3.1 as a marker of prostatic origin in metastatic tumors.NKX3.1作为转移性肿瘤中前列腺起源的标志物。
Am J Surg Pathol. 2010 Aug;34(8):1097-105. doi: 10.1097/PAS.0b013e3181e6cbf3.
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Integrative genomic profiling of human prostate cancer.人类前列腺癌的综合基因组分析。
Cancer Cell. 2010 Jul 13;18(1):11-22. doi: 10.1016/j.ccr.2010.05.026. Epub 2010 Jun 24.
5
A coding-independent function of gene and pseudogene mRNAs regulates tumour biology.基因和假基因 mRNA 的一种无编码依赖性功能调节肿瘤生物学。
Nature. 2010 Jun 24;465(7301):1033-8. doi: 10.1038/nature09144.
6
Regression of castrate-recurrent prostate cancer by a small-molecule inhibitor of the amino-terminus domain of the androgen receptor.雄激素受体氨基端结构域小分子抑制剂抑制去势复发前列腺癌
Cancer Cell. 2010 Jun 15;17(6):535-46. doi: 10.1016/j.ccr.2010.04.027.
7
A constitutively activated form of the p110beta isoform of PI3-kinase induces prostatic intraepithelial neoplasia in mice.PI3-激酶 p110beta 同工型的组成性激活形式可诱导小鼠前列腺上皮内瘤形成。
Proc Natl Acad Sci U S A. 2010 Jun 15;107(24):11002-7. doi: 10.1073/pnas.1005642107. Epub 2010 Jun 1.
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
Dicer ablation impairs prostate stem cell activity and causes prostate atrophy.Dicer 缺失会损害前列腺干细胞活性并导致前列腺萎缩。
Stem Cells. 2010 Jul;28(7):1260-9. doi: 10.1002/stem.455.
10
The human retrovirus XMRV in prostate cancer and chronic fatigue syndrome.人逆转录病毒 XMRV 与前列腺癌和慢性疲劳综合征。
Nat Rev Urol. 2010 Jul;7(7):392-402. doi: 10.1038/nrurol.2010.77. Epub 2010 Jun 1.

前列腺癌的分子遗传学:旧挑战的新展望。

Molecular genetics of prostate cancer: new prospects for old challenges.

机构信息

Department of Medicine, Columbia University Medical Center, New York, New York 10032, USA.

出版信息

Genes Dev. 2010 Sep 15;24(18):1967-2000. doi: 10.1101/gad.1965810.

DOI:10.1101/gad.1965810
PMID:20844012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2939361/
Abstract

Despite much recent progress, prostate cancer continues to represent a major cause of cancer-related mortality and morbidity in men. Since early studies on the role of the androgen receptor that led to the advent of androgen deprivation therapy in the 1940s, there has long been intensive interest in the basic mechanisms underlying prostate cancer initiation and progression, as well as the potential to target these processes for therapeutic intervention. Here, we present an overview of major themes in prostate cancer research, focusing on current knowledge of principal events in cancer initiation and progression. We discuss recent advances, including new insights into the mechanisms of castration resistance, identification of stem cells and tumor-initiating cells, and development of mouse models for preclinical evaluation of novel therapuetics. Overall, we highlight the tremendous research progress made in recent years, and underscore the challenges that lie ahead.

摘要

尽管近年来取得了很大进展,但前列腺癌仍然是男性癌症相关死亡和发病的主要原因。自上世纪 40 年代早期关于雄激素受体作用的研究导致雄激素剥夺疗法问世以来,人们一直对前列腺癌发生和发展的基本机制以及针对这些过程进行治疗干预的潜力有着浓厚的兴趣。在这里,我们介绍了前列腺癌研究的主要主题,重点介绍了癌症发生和发展过程中主要事件的现有知识。我们讨论了最近的进展,包括对去势抵抗机制的新见解、干细胞和肿瘤起始细胞的鉴定,以及用于新型治疗药物临床前评估的小鼠模型的开发。总的来说,我们强调了近年来取得的巨大研究进展,并强调了未来的挑战。