Sakamoto Shinichi, Ichikawa Tomohiko
Nihon Rinsho. 2014 Dec;72(12):2097-102.
Recently, novel anti-androgen and CYP-17 inhibitor have been introduced in clinical practice and significance of androgen mediated pathway is re-acknowledged in basic research of castration resistant prostate cancer (CRPC). Generations of AR splicing variant and/or AR mutation, which result in ligand independent activation of AR, are still primary mechanism of acquiring castration resistance in addition to classical AR amplification. Chromosomal rearrangement through FOXA emerged as novel AR regulating mechanism. TMPRSS2-ERG gene fusion is one of the most prevalent signatures in CRPC. Regulation through non-coding miRNA also play critical role in AR mediated oncogenic pathways. Here we describe the classical and recent topics in basic research of CRPC.
最近，新型抗雄激素药物和CYP-17抑制剂已应用于临床实践，雄激素介导通路的重要性在去势抵抗性前列腺癌（CRPC）的基础研究中再次得到认可。除了经典的雄激素受体（AR）扩增外，导致AR配体非依赖性激活的几代AR剪接变体和/或AR突变仍然是获得去势抵抗的主要机制。通过FOXA发生的染色体重排成为新的AR调节机制。TMPRSS2-ERG基因融合是CRPC中最常见的特征之一。通过非编码微小RNA（miRNA）进行的调控在AR介导的致癌途径中也起着关键作用。在此，我们描述CRPC基础研究中的经典和最新话题。
