@article{oai:kanazawa-u.repo.nii.ac.jp:00014066,
 author = {Mizokami, Atsushi and Namiki, Mikio},
 journal = {Journal of Steroid Biochemistry and Molecular Biology},
 month = {Jan},
 note = {Androgen blockade-naïve prostate cancer (PCa) develops into CRPC during androgen deprivation therapy (ADT) by various genetic actions. The androgen-AR signaling axis plays a key role in this development. PCa cells mainly adapt themselves to the environment of lower androgen concentrations and change into androgen-hypersensitive cells or androgen-independent cells. Androgens of adrenal origin and their metabolites synthesized in the microenvironment in an intracrine/paracrine fashion act on surviving PCa cells and secrete prostate specific antigen (PSA). Total androgen deprivation (TAD) (castration, antiandrogen, and CYP17A1 inhibitor) can become an effective therapeutic strategy concerning the androgen signaling axis-related pathway. However, it is important to ascertain whether elevation of serum PSA results from AR activation or from an androgen-independent tumor volume effect. Then, clinicians can judge it adequately using the imaging studies such as CT or bone scan as well as PSA and bone metabolic markers, an approach which is necessary to judge which treatment is most suitable for the CRPC patients. This article is part of a Special Issue entitled 'Essential role of DHEA'.},
 pages = {164--171},
 title = {Reconsideration of progression to CRPC during androgen deprivation therapy},
 volume = {145},
 year = {2015}
}