Evidence map›Paper›PMID 24798453›Full record

ReviewHormones & cancer2014

The link between androgen receptor splice variants and castration-resistant prostate cancer.

Cynthia C T Sprenger, Stephen R Plymate

Open access · bronzeAbstract readReview
In one paragraph

Review in Hormones & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
8.5field-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

44 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Roles of Splicing Factors in Hormone-Related Cancer Progression.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Article
  16. Strategy for Tumor-Selective Disruption of Androgen Receptor Function in the Spectrum of Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  17. Article
  18. Article
  19. Androgen action in prostate function and disease.American journal of clinical and experimental urology · 2018
    Review
  20. Aldo-Keto Reductase (AKR) 1C3 inhibitors: a patent review.Expert opinion on therapeutic patents · 2017
    Review
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 2 institutions in 1 country.

Cynthia C T SprengerDepartment of Medicine, University of Washington, Seattle, WA, 98104, USA, cts2501@u.washington.edu.
Stephen R Plymate
University of Washington · USVA Puget Sound Health Care System · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PETER S NELSON · 2013 to 2026
$25.0M
Transmembrane Proteases and Prostate CarcinogenesisP01CA085859 · NCI · UNIVERSITY OF WASHINGTON · PI VESSELLA, ROBERT LOUIS · 2002 to 2013
$21.2M
NCI NIH HHS P01 CA085859NCI NIH HHS P01 CA163227NCI NIH HHS P50 CA097186
6 · The paper itself

Abstract

Resistance to the latest advanced prostate cancer therapies, including abiraterone and enzalutamide, is associated with increased expression of constitutively active androgen receptor splice variants (AR-Vs). The exact mechanism by which these therapies result in AR-Vs is unknown, but may include genomic rearrangement of the androgen receptor gene as well as alternative splicing of the AR pre-messenger RNA (mRNA). An additional complication that hinders further development of effective AR strategies is that the mechanisms by which the directed therapies are bypassed may vary. Finally, the question must be addressed as to whether the androgen receptor remains to be the driver of most castration resistant disease or whether truly AR-independent tumors arise after successful androgen ablation therapy. In this review, we will examine androgen receptor splice variants as an alternative mechanism by which prostate cancer becomes resistant to androgen receptor-directed therapy.

Indexed as

Alternative SplicingAnimalsHumansMaleProstatic Neoplasms, Castration-ResistantProtein IsoformsReceptors, AndrogenAR protein, humanProtein IsoformsReceptors, Androgen

Identifiers

PMID24798453
PMCPMC4308035
OpenAlexW2069541720

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.