Evidence map›Paper›PMID 32756332›Full record

ArticleCancers2020

Activation of Epidermal Growth Factor Receptor Sensitizes Glioblastoma Cells to Hypoxia-Induced Cell Death.

Anna-Luisa Luger, Nadja I Lorenz, Hans Urban, Iris Divé, Anna L Engel, Florian Strassheimer, Katja Dettmer, Pia S Zeiner, Shabnam Shaid, Nina Struve and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
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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

16 authors at 4 institutions in 1 country.

Anna-Luisa LugerDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.ORCID 0000-0002-7209-3694
Nadja I LorenzDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Hans UrbanDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Iris DivéDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Anna L EngelDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Florian StrassheimerDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Katja DettmerInstitute of Functional Genomics, University of Regensburg, 93053 Regensburg, Germany.ORCID 0000-0001-7337-2380
Pia S ZeinerDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Shabnam ShaidDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe University, 60590 Frankfurt am Main, Germany.
Nina StruveLaboratory of Radiobiology and Experimental Radiation Oncology, Hubertus Wald Tumorzentrum-University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Malte KriegsLaboratory of Radiobiology and Experimental Radiation Oncology, Hubertus Wald Tumorzentrum-University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Ute HofmannDr. Margarete Fischer-Bosch Institute of Clinical Pharmacology and University of Tübingen, 70376 Stuttgart, Germany.ORCID 0000-0003-0823-9027
Peter J OefnerInstitute of Functional Genomics, University of Regensburg, 93053 Regensburg, Germany.
Patrick N HarterUniversity Cancer Center Frankfurt (UCT), University Hospital Frankfurt, Goethe University, 60590 Frankfurt am Main, Germany.
Joachim P SteinbachDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.
Michael W RonellenfitschDr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, 60528 Frankfurt am Main, Germany.ORCID 0000-0002-1402-6290
Goethe University Frankfurt · DEUniversität Hamburg · DEUniversity of Regensburg · DEDr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology · DE

Funding

ALE has received a scholarship by the Adolf Gutknecht trust. see aboveALL and ID haves received funding from the Medical Faculty of the Goethe University Frankfurt (Frankfurt research funding, FFF) via the program "Patenschaftsmodell" and a fellowship in the program "Clinician Scientist" by the Else Kröner-Fresenius-Stiftun see aboveJ.P.S. and M.W.R. have received funding by the State of Hessen within the LOEWE program. see aboveJPS has received funding by the German Research Foundation (DFG) DFG 2175/1-1MWR has received a fellowship from the University Cancer Center Frankfurt (UCT) as well as from the Medical Faculty of the Goethe University Frankfurt (FFF) via the programs "Nachwuchsforscher" and "Clinician Scientists". see abovePSZ has also received funding from the Medical Faculty of the Goethe University Frankfurt (FFF) via the programs "Patenschaftsmodell" and "Nachwuchsforscher". see aboveThe Dr. Senckenberg Institute of Neurooncology is supported by the Dr. Senckenberg Foundation. see aboveUH is supported by the Robert-Bosch Foundation, Stuttgart, Germany. see above
6 · The paper itself

Abstract

backgroundThe epidermal growth factor receptor (EGFR) signaling pathway is genetically activated in approximately 50% of glioblastomas (GBs). Its inhibition has been explored clinically but produced disappointing results, potentially due to metabolic effects that protect GB cells against nutrient deprivation and hypoxia. Here, we hypothesized that EGFR activation could disable metabolic adaptation and define a GB cell population sensitive to starvation.

methodsUsing genetically engineered GB cells to model different types of EGFR activation, we analyzed changes in metabolism and cell survival under conditions of the tumor microenvironment.

resultsWe found that expression of mutant EGFR

conclusionsThe finding that EGFR activation renders GB cells susceptible to starvation could help to identify a subgroup of patients more likely to benefit from starvation-inducing therapies.

Indexed as

EGFREGFRvIII mutationglioblastomahypoxiastarvation

Identifiers

PMID32756332
PMCPMC7464192
OpenAlexW3046248719

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.