Evidence map›Paper›PMID 27281611›Full record

ArticleOncotarget2016

Radiosensitization of HNSCC cells by EGFR inhibition depends on the induction of cell cycle arrests.

Malte Kriegs, Ulla Kasten-Pisula, Britta Riepen, Konstantin Hoffer, Nina Struve, Laura Myllynen, Friederike Braig, Mascha Binder, Thorsten Rieckmann, Reidar Grénman and 3 more

Open access · diamondAbstract read
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 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  8. Expert reviews in molecular medicine · 2022
    Review
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  11. Review
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  15. Article
  16. The Cell Cycle G2/M Block Is an Indicator of Cellular Radiosensitivity.Dose-response : a publication of International Hormesis Society
    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

13 authors at 4 institutions in 2 countries.

Malte KriegsLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Ulla Kasten-PisulaLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Britta RiepenLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Konstantin HofferLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Nina StruveLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Laura MyllynenLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Friederike BraigDepartment of Oncology and Hematology, BMT with section Pneumology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Mascha BinderDepartment of Oncology and Hematology, BMT with section Pneumology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Thorsten RieckmannLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Reidar GrénmanDepartment of Otorhinolaryngology - Head and Neck Surgery, University of Turku and Turku University Hospital, 20521 Turku, Finland.
Cordula PetersenLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Ekkehard DikomeyLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Kai RothkammLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Universität Hamburg · DEUniversity Cancer Center Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DETurku University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increase in cellular radiosensitivity by EGF receptor (EGFR) inhibition has been shown to be attributable to the induction of a G1-arrest in p53-proficient cells. Because EGFR targeting in combination with radiotherapy is used to treat head and neck squamous cell carcinomas (HNSCC) which are predominantly p53 mutated, we tested the effects of EGFR targeting on cellular radiosensitivity, proliferation, apoptosis, DNA repair and cell cycle control using a large panel of HNSCC cell lines. In these experiments EGFR targeting inhibited signal transduction, blocked proliferation and induced radiosensitization but only in some cell lines and only under normal (pre-plating) conditions. This sensitization was not associated with impaired DNA repair (53BP1 foci) or induction of apoptosis. However, it was associated with the induction of a lasting G2-arrest. Both, the radiosensitization and the G2-arrest were abrogated if the cells were re-stimulated (delayed plating) with actually no radiosensitization being detectable in any of the 14 tested cell lines. Therefore we conclude that EGFR targeting can induce a reversible G2 arrest in p53 deficient HNSCC cells, which does not consequently result in a robust cellular radiosensitization. Together with recent animal and clinical studies our data indicate that EGFR inhibition is no effective strategy to increase the radiosensitivity of HNSCC cells.

Indexed as

Antineoplastic AgentsCarcinoma, Squamous CellCell Cycle CheckpointsCell Line, TumorCetuximabErbB ReceptorsErlotinib HydrochlorideHead and Neck NeoplasmsHumansRadiation ToleranceSquamous Cell Carcinoma of Head and NeckTumor Suppressor Protein p53Antineoplastic AgentsCetuximabEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideTumor Suppressor Protein p53cell cycleEGFRHNSCCradiosensitizationtargeting

Identifiers

PMID27281611
PMCPMC5216710
OpenAlexW2347166984

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.