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. 2019 Sep 4;9:858. doi: 10.3389/fonc.2019.00858

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Copyright © 2019 Feng and He.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Evolution of prostate cancer under androgen deprivation therapy. Androgen sensitive primary prostate cancers arise from prostate luminal epithelial cells, which have undergone genetic alterations, such as mutation of PTEN tumor suppressor (107) or chromosomal rearrangement resulting in the TMPRSS2/ERG chimeric gene (108). Upon androgen deprivation including castration and the first-generation antiandrogen treatment, most HNPC will develop into CRPC, whose survival and growth still depends on androgen receptor signaling. After treatment with more potent androgen deprivation therapies such as second-generation antiandrogens, the majority of CRPC manages to develop novel mechanisms to maintain active androgen signaling axis to confer resistance, whereas a subset of CRPC will irreversibly lose androgen receptor expression, undergo divergent clonal evolution or de-differentiation, and become truly androgen-independent small-cell prostate cancer. ADT, androgen deprivation therapy; HNPC, hormone-naïve prostate cancer; CRPC, castration-resistant prostate cancer; SCPC, small-cell prostate cancer.