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本文引用的文献

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The androgen-regulated protease TMPRSS2 activates a proteolytic cascade involving components of the tumor microenvironment and promotes prostate cancer metastasis.雄激素调节的蛋白酶TMPRSS2激活了一个涉及肿瘤微环境成分的蛋白水解级联反应,并促进前列腺癌转移。
Cancer Discov. 2014 Nov;4(11):1310-25. doi: 10.1158/2159-8290.CD-13-1010. Epub 2014 Aug 13.
2
Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.针对富含纤维母细胞激活蛋白(FAP)的癌相关成纤维细胞中的 CXCL12 进行靶向治疗,与抗 PD-L1 免疫疗法联合应用于胰腺癌。
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Tumor immunotherapy directed at PD-1.针对程序性死亡受体1(PD-1)的肿瘤免疫疗法。
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Hallmarks of cancer: the next generation.癌症的特征:下一代。
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Improved survival with ipilimumab in patients with metastatic melanoma.Ipilimumab 改善转移性黑色素瘤患者的生存。
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The androgen-regulated type II serine protease TMPRSS2 is differentially expressed and mislocalized in prostate adenocarcinoma.雄激素调节的II型丝氨酸蛋白酶TMPRSS2在前列腺腺癌中表达存在差异且定位错误。
J Pathol. 2008 Jun;215(2):118-25. doi: 10.1002/path.2330.
10
Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer.前列腺癌中TMPRSS2与ETS转录因子基因的反复融合
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器官特异性癌症转移机制的见解。

Insights into the mechanism of organ-specific cancer metastasis.

作者信息

Rubin Mark A

机构信息

Institute for Precision Medicine of Weill Cornell Medical College and NewYork-Presbyterian Hospital, New York, New York. Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York. Department of Urology, Weill Cornell Medical College, New York, New York. Meyer Cancer Center of Weill Cornell Medical College and NewYork-Presbyterian Hospital, New York, New York.

出版信息

Cancer Discov. 2014 Nov;4(11):1262-4. doi: 10.1158/2159-8290.CD-14-1075.

DOI:10.1158/2159-8290.CD-14-1075
PMID:25367948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4418487/
Abstract

Lucas and colleagues nominate transmembrane serine protease type II (TMPRSS2) as an important player in the initiation of epithelial-mesenchymal transition (EMT) in prostate cancer. Cancer cells maintain androgen receptor-regulated cytoplasmic TMPRSS2 expression, which facilitates EMT invasion and metastasis in model systems through hepatocyte growth factor and c-MET signaling. In addition to providing a rationale for potentially targeting this organ-specific enabler of metastatic disease progression, this study also highlights the importance of understanding how organ/tissue-specific genes are co-opted in the context of cancer.

摘要

卢卡斯及其同事将II型跨膜丝氨酸蛋白酶(TMPRSS2)确定为前列腺癌上皮-间质转化(EMT)起始过程中的一个重要因素。癌细胞维持雄激素受体调节的细胞质TMPRSS2表达,这在模型系统中通过肝细胞生长因子和c-MET信号促进EMT侵袭和转移。除了为潜在靶向这种转移性疾病进展的器官特异性促成因素提供理论依据外,这项研究还强调了了解器官/组织特异性基因在癌症背景下如何被利用的重要性。