ReviewAmerican journal of clinical and experimental urology2021
Dysregulated androgen synthesis and anti-androgen resistance in advanced prostate cancer.
Review in American journal of clinical and experimental urology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Beyond sex determination: the Y chromosome in male cancers.Nature reviews. Cancer · 2026Review
- Neuroendocrine prostate cancer (NEPC)-associatedCancer pathogenesis and therapy · 2026Article
- The structural basis of aldo-keto reductase 1C3 inhibition by 17α-picolyl and 17(Journal of enzyme inhibition and medicinal chemistry · 2025Article
- In Silico discovery of novel androgen receptor inhibitors for prostate cancer therapy using virtual screening, molecular docking, and molecular dynamics simulations.Scientific reports · 2025Article
- Wnt5a augments intracellular free cholesterol levels and promotes castration resistance in prostate cancer.Journal of translational medicine · 2025Article
- Molecular pathways in reproductive cancers: a focus on prostate and ovarian cancer.Cancer cell international · 2025Review
- Overcoming drug resistance in castrate-resistant prostate cancer: current mechanisms and emerging therapeutic approaches.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Synergistic anticancer effect of CDRI-08 and abiraterone acetate against castration resistant prostate cancer targeting PI3K/Akt pathway.Iranian journal of basic medical sciences · 2025Article
- Therapy resistance in prostate cancer: mechanism, signaling and reversal strategies.Exploration of targeted anti-tumor therapy · 2024Review
- Identification of DNA damage response-related genes as biomarkers for castration-resistant prostate cancer.Scientific reports · 2023Article
- Histone H2A Lys130 acetylation epigenetically regulates androgen production in prostate cancer.Nature communications · 2023Article
- Strategies to Re-Sensitize Castration-Resistant Prostate Cancer to Antiandrogen Therapy.Biomedicines · 2023Review
- A new method to quantify the effect of co-medication on the efficacy of abiraterone in metastatic castration-resistant prostate cancer patients.Frontiers in pharmacology · 2023Article
- Critical Response to Article "Integrated Network Pharmacology and Experimental Validation Approach to Investigate the Mechanisms of Stigmasterol in the Treatment of Rheumatoid Arthritis" [Letter].Drug design, development and therapy · 2023Article
- From Omics to Multi-Omics Approaches for In-Depth Analysis of the Molecular Mechanisms of Prostate Cancer.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current therapies for treating castration resistant prostate cancer (CRPC) include abiraterone and enzalutamide which function by inhibiting androgen signaling by targeting androgen synthesis and antagonizing the androgen receptor (AR) respectively. While these therapies are initially beneficial, resistance inevitably develops. A number of pathways have been identified to contribute to CRPC progression and drug resistance. Among these is aberrant androgen signaling perpetuated by increased expression and activity of androgenic enzymes. While abiraterone inhibits the androgenic enzyme, CYP17A1, androgen synthesis inhibition by abiraterone is incomplete and sustained androgenesis persists, in part due to increased levels of AKR1C3 and steroid sulfatase (STS). Expression of both of these enzymes is increased in CRPC and is associated with resistance to anti-androgens. A number of studies have identified methods for targeting these enzymes. Indomethacin, a non-steroidal anti-inflammatory drug commonly used to treat inflammatory arthritis has been well established as an inhibitor of AKR1C3. Treatment of CRPC cells with indomethacin reduces cell growth and improves the response to enzalutamide and abiraterone. Similarly, STS inhibitors have been shown to reduce intracrine androgens and also reduce CRPC growth and enhance anti-androgen treatment. In this review, we provide an overview of androgen synthesis in CRPC and strategies aimed at inhibiting intracrine androgens.
Indexed as
Identifiers
34541028PMC8446765W3200540246What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.