Evidence map›Paper›PMID 28026145›Full record

ArticleJournal of cellular and molecular medicine2017

The bromodomain inhibitor JQ1 triggers growth arrest and apoptosis in testicular germ cell tumours in vitro and in vivo.

Sina Jostes, Daniel Nettersheim, Martin Fellermeyer, Simon Schneider, François Hafezi, Friedemann Honecker, Valerie Schumacher, Matthias Geyer, Glen Kristiansen, Hubert Schorle

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

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
5.2field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Meta-Analysis of Gene Expressions in Testicular Germ Cell Tumor Histologies.International journal of molecular sciences · 2020
    Pooled it
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  11. Epigenetic Regulation of Driver Genes in Testicular Tumorigenesis.International journal of molecular sciences · 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

10 authors at 3 institutions in 3 countries.

Sina JostesInstitute of Pathology, Department of Developmental Pathology, University Medical School, Bonn, Germany.
Daniel NettersheimInstitute of Pathology, Department of Developmental Pathology, University Medical School, Bonn, Germany.
Martin FellermeyerInstitute of Pathology, Department of Developmental Pathology, University Medical School, Bonn, Germany.
Simon SchneiderInstitute of Pathology, Department of Developmental Pathology, University Medical School, Bonn, Germany.
François HafeziInstitute of Pathology, Department of Developmental Pathology, University Medical School, Bonn, Germany.
Friedemann HoneckerBreast and Tumor Center, ZeTup Silberturm, St Gallen, Switzerland.
Valerie SchumacherDepartment of Urology, Boston Children's Hospital, Boston, MA, USA.
Matthias GeyerInstitute of Innate Immunity, Department of Structural Immunology, University Medical School, Bonn, Germany.
Glen KristiansenInstitute of Pathology, University Medical School, Bonn, Germany.
Hubert SchorleInstitute of Pathology, Department of Developmental Pathology, University Medical School, Bonn, Germany.
University of Bonn · DEBoston Children's Museum · USTumor- und Brustzentrum ZeTuP Silberturm · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type II testicular germ cell cancers (TGCT) are the most frequently diagnosed tumours in young men (20-40 years) and are classified as seminoma or non-seminoma. TGCTs are commonly treated by orchiectomy and chemo- or radiotherapy. However, a subset of metastatic non-seminomas (embryonal carcinomas) displays only incomplete remission or relapse and requires novel treatment options. Recent studies have shown effective application of the small-molecule inhibitor JQ1 in tumour therapy, which interferes with the function of 'bromodomain and extraterminal (BET)' proteins. JQ1-treated TGCT cell lines display up-regulation of genes indicative for DNA damage and cellular stress response and induce cell cycle arrest. Embryonal carcinoma (EC) cell lines, which presented as JQ1 sensitive, display down-regulation of pluripotency factors and induction of mesodermal differentiation. In contrast, seminoma-like TCam-2 cells tolerated higher JQ1 concentrations and were resistant to differentiation. ECs xenografted in vivo showed a reduction in tumour size, proliferation rate and angiogenesis in response to JQ1. Finally, the combination of JQ1 and the histone deacetylase inhibitor romidepsin allowed for lower doses and less frequent application, compared with monotherapy. Thus, we propose that JQ1 in combination with romidepsin may serve as a novel therapeutic option for (mixed) TGCTs.

Indexed as

AdultAnimalsApoptosisAzepinesCell Cycle CheckpointsCell DifferentiationCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasms, Germ Cell and EmbryonalTesticular NeoplasmsTriazolesXenograft Model Antitumor AssaysAzepines(+)-JQ1 compoundTriazolesbromodomain proteinscisplatin resistancedifferentiationepigenetic therapygerm cell cancerHDAC inhibitorJQ1pluripotencyromidepsinxenografts

Identifiers

PMID28026145
PMCPMC5487916
OpenAlexW2562317580

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.