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.
| Original language | English |
|---|---|
| Pages (from-to) | 2090-2094 |
| Number of pages | 5 |
| Journal | Nihon rinsho. Japanese journal of clinical medicine |
| Volume | 72 |
| Issue number | 12 |
| Publication status | Published - Dec 1 2014 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Medicine(all)
Cite this
The concept and mechanisms of castration-resistant prostate cancer. / Naito, Seiji; shiota, masaki.
In: Nihon rinsho. Japanese journal of clinical medicine, Vol. 72, No. 12, 01.12.2014, p. 2090-2094.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - The concept and mechanisms of castration-resistant prostate cancer
AU - Naito, Seiji
AU - shiota, masaki
PY - 2014/12/1
Y1 - 2014/12/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84965187345&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84965187345&partnerID=8YFLogxK
M3 - Review article
C2 - 25518339
AN - SCOPUS:84965187345
VL - 72
SP - 2090
EP - 2094
JO - Astrophysical Journal
JF - Astrophysical Journal
SN - 0004-637X
IS - 12
ER -