Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis.

Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis.
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DOI:
10.1038/ng.371
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发表时间:
2009-05
期刊:
影响因子:
30.8
通讯作者:
Sawyers, Charles L.
Sawyers, Charles L.
中科院分区:
生物学1区
文献类型:
--
作者:
King, Jennifer C.;Xu, Jin;Wongvipat, John;Hieronymus, Haley;Carver, Brett S.;Leung, David H.;Taylor, Barry S.;Sander, Chris;Cardiff, Robert D.;Couto, Suzana S.;Gerald, William L.;Sawyers, Charles L.

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TMPRSS 2-ERG融合存在于50%的前列腺癌中,在前列腺上皮内瘤变(PIN)中不太常见,这引起了关于TMPRSS 2-ERG是否有助于疾病起始的问题。我们确定了一个共同的TMPRSS 2-ERG融合的翻译起始位点,并表明转基因TMPRSS 2-ERG小鼠发展PIN,但仅在PI 3-激酶途径激活的情况下。TMPRSS 2-ERG阳性人肿瘤也富含PTEN丢失,表明在前列腺肿瘤发生中的协同作用。
The TMPRSS2-ERG fusion, present in 50% of prostate cancers, is less common in prostatic intra-epithelial neoplasia (PIN), raising questions about whether TMPRSS2-ERG contributes to disease initiation. We identified the translational start site of a common TMPRSS2-ERG fusion and showed that transgenic TMPRSS2-ERG mice develop PIN, but only in the context of PI3-kinase pathway activation. TMPRSS2-ERG positive human tumors are also enriched for PTEN loss, suggesting cooperation in prostate tumorigenesis.
DOI: 10.1038/ng.370
发表时间: 2009-05
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