Evidence map›Paper›PMID 26537882›Full record

ArticleCurrent treatment options in oncology2015

Clinical Relevance of Androgen Receptor Splice Variants in Castration-Resistant Prostate Cancer.

Benjamin L Maughan, Emmanuel S Antonarakis

Abstract read
PubMed Publisher
In one paragraph

Article in Current treatment options in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Diverse AR-V7 cistromes in castration-resistant prostate cancer are governed by HoxB13.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  8. Androgen Signaling in Prostate Cancer.Cold Spring Harbor perspectives in medicine · 2017
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. New drugs in prostate cancer.Prostate international · 2016
    Review
  15. Review
  16. 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 1 institution in 1 country.

Benjamin L MaughanJohns Hopkins Sidney Kimmel Comprehensive Cancer Center, 1650 Orleans Street, CRB1-1M45, Baltimore, MD, 21287, USA.
Emmanuel S AntonarakisJohns Hopkins Sidney Kimmel Comprehensive Cancer Center, 1650 Orleans Street, CRB1-1M45, Baltimore, MD, 21287, USA. eantona1@jhmi.edu.
Sidney Kimmel Comprehensive Cancer Center · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

opinion statementMetastatic castration-resistant prostate cancer (mCRPC) currently benefits from a wealth of treatment options, yet still remains lethal in the vast majority of patients. It is becoming increasingly understood that this disease entity continues to evolve over time, acquiring additional and diverse resistance mechanisms with each subsequent therapy used. This dynamic relationship between treatment pressure and disease resistance can be challenging for the managing clinician. The recent discovery of alternate splice variants of the androgen receptor (AR) is one potential mechanism of escape in mCRPC, and recognizing this resistance mechanism might be important for optimal treatment selection for our patients. AR-V7 appears to be the most relevant AR splice variant, and early clinical data suggest that it is a negative prognostic marker in mCRPC. Emerging evidence also suggests that detection of AR-V7 may be associated with resistance to novel hormonal therapy (abiraterone and enzalutamide) but may be compatible with sensitivity to taxane chemotherapy (docetaxel and cabazitaxel). Adding to this complexity is the observation that AR-V7 is a dynamic marker whose status may change across time and depending on selective pressures induced by different therapies. Finally, it is possible that AR-V7 may represent a therapeutic target in mCRPC if drugs can be designed that degrade or inhibit AR splice variants or block their transcriptional activity. Several such agents (including galeterone, EPI-506, and bromodomain/BET inhibitors) are now in clinical development.

Indexed as

AndrostenesAndrostenolsBenzamidesBridged-Ring CompoundsDocetaxelDrug Resistance, NeoplasmHumansMaleNitrilesPhenylthiohydantoinProstatic Neoplasms, Castration-ResistantProtein IsoformsReceptors, AndrogenTaxoidsabirateroneAndrostenesAndrostenolsAR protein, humanBenzamidesBridged-Ring CompoundscabazitaxelDocetaxelenzalutamideNitrilesPhenylthiohydantoinProtein IsoformsReceptors, AndrogentaxaneTaxoidsAbirateroneAndrogen receptor variantsAR-V7Castration-resistant prostate cancerEnzalutamideHormonal therapyResistanceTaxane

Identifiers

PMID26537882
OpenAlexW1932786078

What OpenQuestion holds

Textmetadata
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.