Evidence map›Paper›PMID 27322140›Full record

ArticleOncotarget2016

Androgen receptor activity modulates responses to cisplatin treatment in bladder cancer.

Eiji Kashiwagi, Hiroki Ide, Satoshi Inoue, Takashi Kawahara, Yichun Zheng, Leonardo O Reis, Alexander S Baras, Hiroshi Miyamoto

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.0field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
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  12. The androgen receptor in bladder cancer.Nature reviews. Urology · 2023
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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

8 authors at 2 institutions in 1 country.

Eiji KashiwagiDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hiroki IdeDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Satoshi InoueDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Takashi KawaharaDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yichun ZhengDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Leonardo O ReisDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Alexander S BarasDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hiroshi MiyamotoDepartments of Pathology and Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin (CDDP)-based combination chemotherapy remains the mainstream treatment for advanced bladder cancer. However, its efficacy is often limited due to the development of resistance for which underlying mechanisms are poorly understood. Meanwhile, emerging evidence has indicated the involvement of androgen-mediated androgen receptor (AR) signals in bladder cancer progression. In this study, we aimed to investigate whether AR signals have an impact on sensitivity to CDDP in bladder cancer cells. UMUC3-control-short hairpin RNA (shRNA) cells with endogenous AR and AR-negative 647V/5637 cells stably expressing AR were significantly more resistant to CDDP treatment at its pharmacological concentrations, compared with UMUC3-AR-shRNA and 647V-vector/5637-vector control cells, respectively. A synthetic androgen R1881 significantly reduced CDDP sensitivity in UMUC3, 647V-AR, or 5637-AR cells, and the addition of an anti-androgen hydroxyflutamide inhibited the effect of R1881. In these AR-positive cells, R1881 treatment also induced the expression levels of NF-κB, which is known to involve CDDP resistance, and its phosphorylated form, as well as nuclear translocation of NF-κB. In CDDP-resistant bladder cancer sublines established following long-term culture with CDDP, the expression levels of AR as well as NF-κB and phospho-NF-κB were considerably elevated, compared with respective control sublines. In bladder cancer specimens, there was a strong trend to correlate between AR positivity and chemoresistance. These results suggest that AR activation correlates with CDDP resistance presumably via modulating NF-κB activity in bladder cancer cells. Targeting AR during chemotherapy may thus be a useful strategy to overcome CDDP resistance in patients with AR-positive bladder cancer.

Indexed as

Drug Resistance, NeoplasmCell Line, TumorCisplatinFemaleHumansImmunohistochemistryMaleNF-kappa BPhosphorylationReceptors, AndrogenRNA, Small InterferingSignal TransductionTreatment OutcomeUrinary Bladder NeoplasmsCisplatinNF-kappa BReceptors, AndrogenRNA, Small Interferingandrogen receptorbladder cancerchemoresistancecisplatinNF-κB

Identifiers

PMID27322140
PMCPMC5226499
OpenAlexW2426061205

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.