TMPRSS2-ERG的协同作用与PI3激酶通路激活在前列腺癌发生中的作用
Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis.
作者信息
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
机构信息
Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
出版信息
Nat Genet. 2009 May;41(5):524-6. doi: 10.1038/ng.371. Epub 2009 Apr 26.
Abstract
The TMPRSS2-ERG fusion, present in approximately 50% of prostate cancers, is less common in prostatic intraepithelial 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.
摘要
TMPRSS2-ERG融合在大约50%的前列腺癌中存在，而在前列腺上皮内瘤变（PIN）中则较少见，这引发了关于TMPRSS2-ERG是否促成疾病起始的疑问。我们确定了一种常见TMPRSS2-ERG融合的翻译起始位点，并表明转基因TMPRSS2-ERG小鼠会发生PIN，但仅在PI3激酶途径激活的情况下。TMPRSS2-ERG阳性的人类肿瘤中PTEN缺失也很常见，提示其在前列腺肿瘤发生过程中存在协同作用。
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