Evidence map›Paper›PMID 26331358›Full record

ReviewClinical pharmacology and therapeutics2015

Androgen receptor targeting drugs in castration-resistant prostate cancer and mechanisms of resistance.

D J Crona, M I Milowsky, Y E Whang

Open access · greenAbstract readReview
In one paragraph

Review in Clinical pharmacology and therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Citrullination and the protein code: crosstalk between post-translational modifications in cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Antagonizing CD105 and androgen receptor to target stromal-epithelial interactions for clinical benefit.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  17. Article
  18. Article
  19. The Role of Theranostics in Prostate Cancer.Seminars in radiation oncology · 2021
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

D J CronaDivision of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina, USA.
M I MilowskyDivision of Hematology and Oncology, Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA.
Y E WhangDivision of Hematology and Oncology, Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA.
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
UNC-Duke Collaborative Clinical Pharmacology Postdoctoral Training Program-Evaluation SupplementT32GM086330 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KIM L.R. BROUWER, Daniel Gonzalez · 2011 to 2026
$8.5M
NCI NIH HHS P30 CA016086NIGMS NIH HHS T32 GM086330NIGMS NIH HHS T32GM086330
6 · The paper itself

Abstract

Reactivated androgen receptor (AR) signaling drives castration-resistant prostate cancer (CRPC). The novel AR targeting drugs abiraterone and enzalutamide have improved survival of CRPC patients. However, resistance to these agents develops and patients ultimately succumb to CRPC. Potential mechanisms of resistance include the following: 1) Expression of AR splice variants, such as the AR-V7 isoform, which lacks the ligand-binding domain; 2) AR missense mutations in the ligand-binding domain, such as F876L and T877A; and 3) Mutation or overexpression of androgen biosynthetic enzymes or glucocorticoid receptor. Several novel agents may overcome resistance mechanisms. Galeterone acts through multiple mechanisms that include degradation of AR protein and is being evaluated in CRPC patients positive for AR-V7. EPI-001 and related compounds inhibit AR splice variants by targeting the N-terminal transactivation domain of AR. Promising therapies and novel biomarkers, such as AR-V7, may lead to improved outcomes for CRPC patients.

Indexed as

Drug Resistance, NeoplasmAndrogen Receptor AntagonistsAnimalsAntineoplastic Agents, HormonalHumansLigandsMaleMolecular Targeted TherapyNeoplasms, Hormone-DependentProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionTreatment OutcomeAndrogen Receptor AntagonistsAntineoplastic Agents, HormonalAR protein, humanLigandsReceptors, Androgen

Identifiers

PMID26331358
PMCPMC4715745
OpenAlexW1962442902

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.