Evidence map›Paper›PMID 28264478›Full record

ReviewCancers2017

Crosstalk of the Androgen Receptor with Transcriptional Collaborators: Potential Therapeutic Targets for Castration-Resistant Prostate Cancer.

Daisuke Obinata, Kenichi Takayama, Satoru Takahashi, Satoshi Inoue

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.7field-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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
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  7. Article
  8. Review
  9. Review
  10. Review
  11. Molecular Mechanisms of DUBs Regulation in Signaling and Disease.International journal of molecular sciences · 2021
    Review
  12. Scaffold attachment factor B1 regulates androgen degradation pathways in prostate cancer.American journal of clinical and experimental urology · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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  20. 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

4 authors at 3 institutions in 1 country.

Daisuke ObinataDepartment of Urology, Nihon University School of Medicine, Tokyo 173-8610, Japan. obinata.daisuke@nihon-u.ac.jp.
Kenichi TakayamaDepartment of Functional Biogerontology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan. ktakayama-tky@umin.ac.jp.
Satoru TakahashiDepartment of Urology, Nihon University School of Medicine, Tokyo 173-8610, Japan. takahashi.satoru@nihon-u.ac.jp.
Satoshi InoueDepartment of Functional Biogerontology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan. sinoue@tmig.or.jp.
Tokyo Metropolitan Institute of Gerontology · JPNihon University · JPSaitama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the second leading cause of death from cancer among males in Western countries. It is also the most commonly diagnosed male cancer in Japan. The progression of prostate cancer is mainly influenced by androgens and the androgen receptor (AR). Androgen deprivation therapy is an established therapy for advanced prostate cancer; however, prostate cancers frequently develop resistance to low testosterone levels and progress to the fatal stage called castration-resistant prostate cancer (CRPC). Surprisingly, AR and the AR signaling pathway are still activated in most CRPC cases. To overcome this problem, abiraterone acetate and enzalutamide were introduced for the treatment of CRPC. Despite the impact of these drugs on prolonged survival, CRPC acquires further resistance to keep the AR pathway activated. Functional molecular studies have shown that some of the AR collaborative transcription factors (TFs), including octamer transcription factor (OCT1), GATA binding protein 2 (GATA2) and forkhead box A1 (FOXA1), still stimulate AR activity in the castration-resistant state. Therefore, elucidating the crosstalk between the AR and collaborative TFs on the AR pathway is critical for developing new strategies for the treatment of CRPC. Recently, many compounds targeting this pathway have been developed for treating CRPC. In this review, we summarize the AR signaling pathway in terms of AR collaborators and focus on pyrrole-imidazole (PI) polyamide as a candidate compound for the treatment of prostate cancer.

Indexed as

androgen receptorandrogen receptor signaling pathwaycoregulatoroctamer transcription factor 1pyrrole-imidazole polyamide

Identifiers

PMID28264478
PMCPMC5366817
OpenAlexW2592736267

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.