Exploring anti-androgen therapies in hormone dependent prostate cancer and new therapeutic routes for castration resistant prostate cancer.
PARP inhibitors
Therapy
anti-androgen
castration resistant prostate cancer
epigenetic targeted treatment
Journal
Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782
Informations de publication
Date de publication:
2022
2022
Historique:
received:
09
08
2022
accepted:
16
09
2022
entrez:
20
10
2022
pubmed:
21
10
2022
medline:
22
10
2022
Statut:
epublish
Résumé
Androgen deprivation therapies (ADTs) are important treatments which inhibit androgen-induced prostate cancer (PCa) progression by either preventing androgen biosynthesis (e.g. abiraterone) or by antagonizing androgen receptor (AR) function (e.g. bicalutamide, enzalutamide, darolutamide). A major limitation of current ADTs is they often remain effective for limited durations after which patients commonly progress to a lethal and incurable form of PCa, called castration-resistant prostate cancer (CRPC) where the AR continues to orchestrate pro-oncogenic signalling. Indeed, the increasing numbers of ADT-related treatment-emergent neuroendocrine-like prostate cancers (NePC), which lack AR and are thus insensitive to ADT, represents a major therapeutic challenge. There is therefore an urgent need to better understand the mechanisms of AR action in hormone dependent disease and the progression to CRPC, to enable the development of new approaches to prevent, reverse or delay ADT-resistance. Interestingly the AR regulates distinct transcriptional networks in hormone dependent and CRPC, and this appears to be related to the aberrant function of key AR-epigenetic coregulator enzymes including the lysine demethylase 1 (LSD1/KDM1A). In this review we summarize the current best status of anti-androgen clinical trials, the potential for novel combination therapies and we explore recent advances in the development of novel epigenetic targeted therapies that may be relevant to prevent or reverse disease progression in patients with advanced CRPC.
Identifiants
pubmed: 36263323
doi: 10.3389/fendo.2022.1006101
pmc: PMC9575553
doi:
Substances chimiques
Receptors, Androgen
0
Androgen Antagonists
0
Lysine
K3Z4F929H6
Androgens
0
Histone Demethylases
EC 1.14.11.-
KDM1A protein, human
EC 1.5.-
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1006101Informations de copyright
Copyright © 2022 Harris, Metzler, Lothion-Roy, Varun, Woodcock, Haigh, Endeley, Haque, Toss, Alsaleem, Persson, Gudas, Rakha, Robinson, Khani, Martin, Moyer, Brownlie, Madhusudan, Allegrucci, James, Rutland, Fray, Ntekim, de Brot, Mongan and Jeyapalan.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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