title: [The concept and mechanisms of castration-resistant prostate cancer].
abstract: 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.
authors.forename: Seiji
authors.initials: S
authors.lastname: Naito
authors.forename: Masaki
authors.initials: M
authors.lastname: Shiota
mesh_terms: D000728:Androgens / Q000096:biosynthesis; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008297:Male; D009154:Mutation; D064129:Prostatic Neoplasms, Castration-Resistant / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D011499:Protein Processing, Post-Translational; D011944:Receptors, Androgen / Q000235:genetics / Q000378:metabolism
chemical_list: D000728:Androgens; D011944:Receptors, Androgen