title: [Current status of castration resistant prostate cancer basic research].
abstract: 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.
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sakamoto
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Ichikawa
mesh_terms: D017398:Alternative Splicing; D015321:Gene Rearrangement; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics; D009154:Mutation; D064129:Prostatic Neoplasms, Castration-Resistant / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D011944:Receptors, Androgen / Q000235:genetics / Q000378:metabolism
chemical_list: D035683:MicroRNAs; D011944:Receptors, Androgen