Evidence map›Paper›PMID 27725309›Full record

ReviewPharmacological research2016

Androgen receptor variation affects prostate cancer progression and drug resistance.

Edel McCrea, Tristan M Sissung, Douglas K Price, Cindy H Chau, William D Figg

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacological research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Alternative RNA splicing defects in pediatric cancers: new insights in tumorigenesis and potential therapeutic vulnerabilities.Annals of oncology : official journal of the European Society for Medical Oncology · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Diosgenin inhibits the expression of NEDD4 in prostate cancer cells.American journal of translational research · 2019
    Article
  14. Alternative splicing in prostate cancer.Nature reviews. Clinical oncology · 2018
    Review
  15. Article
  16. Precision medicine applications in prostate cancer.Therapeutic advances in medical oncology · 2018
    Review
  17. Article
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Edel McCreaMolecular Pharmacology Section, Genitourinary Malignancies Branch, National Cancer Institute, Bethesda, MD, United States.
Tristan M SissungThe Clinical Pharmacology Program, Office of the Clinical Director, National Cancer Institute, Bethesda, MD, United States.
Douglas K PriceMolecular Pharmacology Section, Genitourinary Malignancies Branch, National Cancer Institute, Bethesda, MD, United States.
Cindy H ChauMolecular Pharmacology Section, Genitourinary Malignancies Branch, National Cancer Institute, Bethesda, MD, United States.
William D FiggMolecular Pharmacology Section, Genitourinary Malignancies Branch, National Cancer Institute, Bethesda, MD, United States; The Clinical Pharmacology Program, Office of the Clinical Director, National Cancer Institute, Bethesda, MD, United States. Electronic address: wdfigg@helix.nih.gov.
National Cancer Institute · US

Funding

Identify SNPs and Polymorphisms Involved in the Development of Prostate CancerZIABC010453 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2009 to 2025
$10.4M
Drug Development for Prostate Cancer and other Metastatic ProcessesZIABC010547 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2009 to 2025
$10.2M
Intramural NIH HHS ZIA BC010547
6 · The paper itself

Abstract

Significant therapeutic progress has been made in treating prostate cancer in recent years. Drugs such as enzalutamide, abiraterone, and cabazitaxel have expanded the treatment armamentarium, although it is not completely clear which of these drugs are the most-effective option for individual patients. Moreover, such advances have been tempered by the development of therapeutic resistance. The purpose of this review is to summarize the current literature pertaining to the biochemical effects of AR variants and their consequences on prostate cancer therapies at both the molecular level and in clinical treatment. We address how these AR splice variants and mutations affect tumor progression and therapeutic resistance and discuss potential novel therapeutic strategies under development. It is hoped that these therapies can be administered with increasing precision as tumor genotyping methods become more sophisticated, thereby lending clinicians a better understanding of the underlying biology of prostate tumors in individual patients.

Indexed as

Drug Resistance, NeoplasmGenetic VariationAnimalsAntineoplastic AgentsDisease ProgressionGenotypeHumansMaleMutationProstateProstatic NeoplasmsReceptors, AndrogenAntineoplastic AgentsAR protein, humanReceptors, AndrogenAndrogen receptorAR-V7MutationPharmacologyProstate cancer

Identifiers

PMID27725309
PMCPMC5154811
OpenAlexW2528268830

What OpenQuestion holds

Textmetadata
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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.