Evidence map›Paper›PMID 23762372›Full record

ArticlePloS one2013

Screening for EGFR amplifications with a novel method and their significance for the outcome of glioblastoma patients.

Michał Bieńkowski, Sylwester Piaskowski, Ewelina Stoczyńska-Fidelus, Małgorzata Szybka, Mateusz Banaszczyk, Monika Witusik-Perkowska, Emilia Jesień-Lewandowicz, Dariusz J Jaskólski, Anna Radomiak-Załuska, Dorota Jesionek-Kupnicka and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. HeterogeneousCancers · 2020
    Article
  13. Article
  14. Article
  15. Biomarkers for glioblastoma multiforme: status quo.Journal of clinical and translational research · 2016
    Review
  16. Article
  17. Article
  18. Extracellular vesicles shed by glioma cells: pathogenic role and clinical value.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
  19. Article
  20. Article
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

14 authors at 1 institution in 1 country.

Michał BieńkowskiDepartment of Molecular Pathology and Neuropathology, Chair of Oncology, Medical University of Lodz, Lodz, Poland. michal.bienkowski@gmail.com
Sylwester Piaskowski
Ewelina Stoczyńska-Fidelus
Małgorzata Szybka
Mateusz Banaszczyk
Monika Witusik-Perkowska
Emilia Jesień-Lewandowicz
Dariusz J Jaskólski
Anna Radomiak-Załuska
Dorota Jesionek-Kupnicka
Beata Sikorska
Wielisław Papierz
Piotr Rieske
Paweł P Liberski
Medical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is a highly aggressive tumour of the central nervous system, characterised by poor prognosis irrespective of the applied treatment. The aim of our study was to analyse whether the molecular markers of glioblastoma (i.e. TP53 and IDH1 mutations, CDKN2A deletion, EGFR amplification, chromosome 7 polysomy and EGFRvIII expression) could be associated with distinct prognosis and/or response to the therapy. Moreover, we describe a method which allows for a reliable, as well as time- and cost-effective, screening for EGFR amplification and chromosome 7 polysomy with quantitative Real-Time PCR at DNA level. In the clinical data, only the patient's age had prognostic significance (continuous: HR = 1.04; p<0.01). At the molecular level, EGFRvIII expression was associated with a better prognosis (HR = 0.37; p = 0.04). Intriguingly, EGFR amplification was associated with a worse outcome in younger patients (HR = 3.75; p<0.01) and in patients treated with radiotherapy (HR = 2.71; p = 0.03). We did not observe any difference between the patients with the amplification treated with radiotherapy and the patients without such a treatment. Next, EGFR amplification was related to a better prognosis in combination with the homozygous CDKN2A deletion (HR = 0.12; p = 0.01), but to a poorer prognosis in combination with chromosome 7 polysomy (HR = 14.88; p = 0.01). Importantly, the results emphasise the necessity to distinguish both mechanisms of the increased EGFR gene copy number (amplification and polysomy). To conclude, although the data presented here require validation in different groups of patients, they strongly advocate the consideration of the patient's tumour molecular characteristics in the selection of the therapy.

Indexed as

AdultAgedAged, 80 and overAge FactorsAntineoplastic AgentsBiomarkers, TumorBrain NeoplasmsChromosome AberrationsChromosomes, Human, Pair 7Cyclin-Dependent Kinase Inhibitor p16DNA Copy Number VariationsErbB ReceptorsFemaleGamma RaysGene DeletionGenetic TestingAntineoplastic AgentsBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16EGFR protein, humanErbB Receptors

Identifiers

PMID23762372
PMCPMC3675194
OpenAlexW1985417291

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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.