Naito Seiji, Shiota Masaki
Nihon Rinsho. 2014 Dec;72(12):2090-4.
Castration-resistant prostate cancer (CRPC) is the term which has recently been raised instead of androgen-independent or hormone-refractory prostate cancer. CRPC is defined as the status of disease progression despite the serum testosterone level of castration (< 50 ng/mL), which can be caused by various mechanisms including androgen receptor (AR)-dependent and AR-independent pathways. Recent researches have revealed that aberrant activation of AR signaling due to ectopic androgen synthesis, AR amplification, AR overexpression, AR mutation, AR variant, AR cofactor, and AR post-translational modification is a key mechanism of CRPC. In addition, AR-independent pathway can contribute to the emergence of CRPC. Taken together, it has been thought that these various mechanisms heterogeneously make androgen-dependent to castration resistant in a spatiotemporal-specific manner.
去势抵抗性前列腺癌（CRPC）是最近提出的术语，用以取代雄激素非依赖性或激素难治性前列腺癌。CRPC被定义为尽管血清睾酮水平处于去势状态（<50 ng/mL）但疾病仍进展的情况，其可由多种机制引起，包括雄激素受体（AR）依赖性和AR非依赖性途径。最近的研究表明，由于异位雄激素合成、AR扩增、AR过表达、AR突变、AR变体、AR辅因子和AR翻译后修饰导致的AR信号异常激活是CRPC的关键机制。此外，AR非依赖性途径也可促使CRPC的出现。综上所述，人们认为这些不同的机制以时空特异性的方式使雄激素依赖性转变为去势抵抗性。
