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 |
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All Science Journal Classification (ASJC) codes
- Medicine(all)
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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.
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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 -