PMID- 24717975
OWN - NLM
STAT- MEDLINE
DCOM- 20150223
LR  - 20181202
IS  - 1879-1220 (Electronic)
IS  - 0960-0760 (Linking)
VI  - 145
DP  - 2015 Jan
TI  - Reconsideration of progression to CRPC during androgen deprivation therapy.
PG  - 164-71
LID - S0960-0760(14)00086-7 [pii]
LID - 10.1016/j.jsbmb.2014.03.015 [doi]
AB  - Androgen blockade-naive 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'.
CI  - Copyright (c) 2014 Elsevier Ltd. All rights reserved.
FAU - Mizokami, Atsushi
AU  - Mizokami A
AD  - Department of Integrative Cancer Therapy and Urology, Kanazawa University 
      Graduate School of Medical Sciences, 13-1 Takaramachi, Kanazawa, Ishikawa 
      920-8640, Japan. Electronic address: mizokami@med.kanazawa-u.ac.jp.
FAU - Namiki, Mikio
AU  - Namiki M
AD  - Department of Integrative Cancer Therapy and Urology, Kanazawa University 
      Graduate School of Medical Sciences, 13-1 Takaramachi, Kanazawa, Ishikawa 
      920-8640, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140406
PL  - England
TA  - J Steroid Biochem Mol Biol
JT  - The Journal of steroid biochemistry and molecular biology
JID - 9015483
RN  - 0 (AR protein, human)
RN  - 0 (Androgen Antagonists)
RN  - 0 (Androgens)
RN  - 0 (Receptors, Androgen)
RN  - 0 (Steroids)
RN  - 0 (Taxoids)
RN  - 15H5577CQD (Docetaxel)
RN  - 459AG36T1B (Dehydroepiandrosterone)
RN  - EC 3.4.21.77 (Prostate-Specific Antigen)
SB  - IM
MH  - Androgen Antagonists/therapeutic use
MH  - Androgens/*metabolism
MH  - Dehydroepiandrosterone/*metabolism
MH  - Disease Progression
MH  - Docetaxel
MH  - Humans
MH  - Male
MH  - Prostate-Specific Antigen/metabolism
MH  - Prostatic Neoplasms/*drug therapy/pathology
MH  - Prostatic Neoplasms, Castration-Resistant/*drug therapy/pathology
MH  - Receptors, Androgen/metabolism
MH  - Signal Transduction
MH  - Steroids/metabolism
MH  - Taxoids/therapeutic use
OTO - NOTNLM
OT  - Androgen deprivation therapy
OT  - CRPC
OT  - DHEA
OT  - Mechanism
EDAT- 2014/04/11 06:00
MHDA- 2015/02/24 06:00
CRDT- 2014/04/11 06:00
PHST- 2014/02/14 00:00 [received]
PHST- 2014/03/19 00:00 [revised]
PHST- 2014/03/28 00:00 [accepted]
PHST- 2014/04/11 06:00 [entrez]
PHST- 2014/04/11 06:00 [pubmed]
PHST- 2015/02/24 06:00 [medline]
AID - S0960-0760(14)00086-7 [pii]
AID - 10.1016/j.jsbmb.2014.03.015 [doi]
PST - ppublish
SO  - J Steroid Biochem Mol Biol. 2015 Jan;145:164-71. doi: 
      10.1016/j.jsbmb.2014.03.015. Epub 2014 Apr 6.