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Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer.

机译:小鼠Pten肿瘤抑制基因的前列腺特异性缺失导致转移性前列腺癌。

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The murine Pten prostate cancer model described in this study recapitulates the disease progression seen in humans: initiation of prostate cancer with prostatic intraepithelial neoplasia (PIN), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Furthermore, while Pten null prostate cancers regress after androgen ablation, they are capable of proliferating in the absence of androgen. Global assessment of molecular changes caused by homozygous Pten deletion identified key genes known to be relevant to human prostate cancer, including those "signature" genes associated with human cancer metastasis. This murine prostate cancer model provides a unique tool for both exploring the molecular mechanism underlying prostate cancer and for development of new targeted therapies.
机译:这项研究中描述的鼠类Pten前列腺癌模型概括了人类所见的疾病进展:前列腺癌开始于前列腺上皮内瘤变(PIN),然后发展为浸润性腺癌,随后转移具有确定的动力学。此外,尽管Pten无效前列腺癌在雄激素消融后会消退,但它们在没有雄激素的情况下仍能增殖。由纯合Pten缺失引起的分子变化的全球评估确定了已知与人类前列腺癌相关的关键基因,包括那些与人类癌症转移相关的“签名”基因。这种鼠类前列腺癌模型为探索前列腺癌的分子机制和开发新的靶向疗法提供了独特的工具。

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