» Articles » PMID: 23247694

Adaptation or Selection--mechanisms of Castration-resistant Prostate Cancer

Overview
Journal Nat Rev Urol
Specialty Urology
Date 2012 Dec 19
PMID 23247694
Citations 66
Authors
Affiliations
Soon will be listed here.
Abstract

Men with advanced prostate cancer are typically treated with hormonal therapy, which leads to tumour shrinkage. However, tumours relapse and develop into the lethal form of the disease, termed castration-resistant prostate cancer (CRPC). Two distinct, but not mutually exclusive, models have been proposed in the literature to describe the onset of CRPC: adaptation and selection. Although some studies indicate that tumour cells acquire new alterations that enable them to survive in the castrated state (adaptation), other research points to the outgrowth of rare, pre-existing cells capable of surviving hormonal therapy (selection). Targeting the cells that survive hormonal therapy--by either adaptation or selection--is necessary to prevent the development of CRPC. Current research is focused on not only understanding the cellular mechanisms of CRPC, but also defining critical pathways that can be targeted with combinatorial therapies in castration-resistant cancer cells.

Citing Articles

Development of an orally bioavailable CDK12/13 degrader and induction of synthetic lethality with AKT pathway inhibition.

Chang Y, Wang X, Yang J, Tien J, Mannan R, Cruz G Cell Rep Med. 2024; 5(10):101752.

PMID: 39353441 PMC: 11513842. DOI: 10.1016/j.xcrm.2024.101752.


Epigenetic roles of KDM3B and KDM3C in tumorigenesis and their therapeutic implications.

Yoo J, Kim G, Jeon Y, Lee S, Kwon S Cell Death Dis. 2024; 15(6):451.

PMID: 38926399 PMC: 11208531. DOI: 10.1038/s41419-024-06850-z.


Endoplasmic reticulum stress-related genes as prognostic and immunogenic biomarkers in prostate cancer.

Wan L, Fan Y, Wu T, Liu Y, Zhang R, Chen S Eur J Med Res. 2024; 29(1):242.

PMID: 38643190 PMC: 11031923. DOI: 10.1186/s40001-024-01818-3.


MiR26a reverses enzalutamide resistance in a bone-tumor targeted system with an enhanced effect on bone metastatic CRPC.

Wang Y, Chen J, Gong L, Wang Y, Siltari A, Lou Y J Nanobiotechnology. 2024; 22(1):145.

PMID: 38566211 PMC: 10985917. DOI: 10.1186/s12951-024-02438-z.


Exploring the resistance mechanism of triple-negative breast cancer to paclitaxel through the scRNA-seq analysis.

Gao W, Sun L, Gai J, Cao Y, Zhang S PLoS One. 2024; 19(1):e0297260.

PMID: 38227591 PMC: 10791000. DOI: 10.1371/journal.pone.0297260.


References
1.
Glickman M, Sawyers C . Converting cancer therapies into cures: lessons from infectious diseases. Cell. 2012; 148(6):1089-98. PMC: 3465702. DOI: 10.1016/j.cell.2012.02.015. View

2.
Marcelli M, Ittmann M, Mariani S, Sutherland R, Nigam R, Murthy L . Androgen receptor mutations in prostate cancer. Cancer Res. 2000; 60(4):944-9. View

3.
Choi N, Zhang B, Zhang L, Ittmann M, Xin L . Adult murine prostate basal and luminal cells are self-sustained lineages that can both serve as targets for prostate cancer initiation. Cancer Cell. 2012; 21(2):253-65. PMC: 3285423. DOI: 10.1016/j.ccr.2012.01.005. View

4.
Germann M, Wetterwald A, Guzman-Ramirez N, van der Pluijm G, Culig Z, Cecchini M . Stem-like cells with luminal progenitor phenotype survive castration in human prostate cancer. Stem Cells. 2012; 30(6):1076-86. DOI: 10.1002/stem.1087. View

5.
Mizokami A, Koh E, Fujita H, Maeda Y, Egawa M, Koshida K . The adrenal androgen androstenediol is present in prostate cancer tissue after androgen deprivation therapy and activates mutated androgen receptor. Cancer Res. 2004; 64(2):765-71. DOI: 10.1158/0008-5472.can-03-0130. View