Evidence map›Paper›PMID 26566796›Full record

ReviewJournal of hematology & oncology2015

Persistent androgen receptor addiction in castration-resistant prostate cancer.

Michael T Schweizer, Evan Y Yu

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03863145 (Open Label, Multicenter, Phase 1 Study to Evaluate the Maximum Tolerated Dose of Orally Administered CB-03-10 With Dose Expansion Phase, in Subjects With Advanced Solid Tumors), which is not on this map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 3% 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.

NCT03863145 early_phase1unknown statusnot on this mapstarted 2022, after this paper: background citation

Open Label, Multicenter, Phase 1 Study to Evaluate the Maximum Tolerated Dose of Orally Administered CB-03-10 With Dose Expansion Phase, in Subjects With Advanced Solid Tumors

TypeinterventionalSponsorCosmo Technologies LtdRan2022 to 2026Enrolled90ConditionsAdvanced Refractory Solid Tumors, Subjects Considered Likely to Respond to CB-03-10ArmsCB-03-10
3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. CBP/p300, a promising therapeutic target for prostate cancer.Journal of translational medicine · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Transcriptomic Profiles ofInternational journal of molecular sciences · 2023
    Article
  16. Review
  17. Review
  18. Pyrogallol fromInternational journal of molecular sciences · 2023
    Article
  19. 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

2 authors at 1 institution in 1 country.

Michael T SchweizerDivision of Oncology, Department of Medicine, University of Washington/Fred Hutchinson Cancer Research Center, Seattle, WA, 98109, USA. schweize@uw.edu.
Evan Y YuDivision of Oncology, Department of Medicine, University of Washington/Fred Hutchinson Cancer Research Center, Seattle, WA, 98109, USA. evanyu@u.washington.edu.
University of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is now understood that persistent activation of the androgen receptor (AR) signaling pathway often underlies the development of castration-resistant prostate cancer (CRPC). This realization led to renewed interest in targeting the AR and ultimately to the development of the potent next-generation AR-directed agents abiraterone and enzalutamide. While these drugs prolong survival in men with CRPC, they are unfortunately not curative. Perhaps not surprisingly, evidence points to persistent AR signaling as one of the key drivers by which resistances to these agents develops. In this context, activation of the AR signaling program can occur through a number of molecular adaptations, including alterations leading to persistent canonical AR signaling (e.g., AR amplification/overexpression, elucidations/concentration of intratumoral androgens), activation of the AR program via feedback pathways (e.g., AKT/mTOR/Pi3K, HER2/Neu), and activation of the AR program via mutation or substitution (e.g., AR ligand binding domain mutation; AR splice variants; glucocorticoid receptor signaling). This review will provide an overview of the more clinical relevant (i.e., druggable) pathways that have been implicated in the emergence of drug resistance in men with CRPC and highlight some of the ongoing efforts towards developing therapeutics to impair these mechanisms.

Indexed as

Androgen AntagonistsAndrostenesAntineoplastic AgentsBenzamidesFeedback, PhysiologicalHumansMaleNitrilesPhenylthiohydantoinProstatic Neoplasms, Castration-ResistantReceptors, AndrogenabirateroneAndrogen AntagonistsAndrostenesAntineoplastic AgentsAR protein, humanBenzamidesenzalutamideNitrilesPhenylthiohydantoinReceptors, Androgen

Identifiers

PMID26566796
PMCPMC4644296
OpenAlexW2176061850

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.