Wang Shunyou, Gao Jing, Lei Qunying, Rozengurt Nora, Pritchard Colin, Jiao Jing, Thomas George V, Li Gang, Roy-Burman Pradip, Nelson Peter S, Liu Xin, Wu Hong
Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, 90095, Los Angeles, CA, USA
Cancer Cell. 2003 Sep;4(3):209-21. doi: 10.1016/s1535-6108(03)00215-0.
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.
本研究中描述的小鼠Pten前列腺癌模型概括了人类疾病的进展情况：前列腺上皮内瘤变（PIN）引发前列腺癌，随后发展为浸润性腺癌，并以特定动力学发生转移。此外，虽然Pten缺失的前列腺癌在雄激素去除后会消退，但它们能够在无雄激素的情况下增殖。对纯合Pten缺失引起的分子变化进行整体评估，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“标志性”基因。这种小鼠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治疗提供了独特的工具。
