Evidence map›Paper›PMID 25245676›Full record

ArticleOncotarget2014

Inhibition of SphK1 reduces radiation-induced migration and enhances sensitivity to cetuximab treatment by affecting the EGFR / SphK1 crosstalk.

Carlotta Schiefler, Guido Piontek, Johannes Doescher, Dominik Schuettler, Martin Mißlbeck, Martina Rudelius, Anna Haug, Rudolf Reiter, Gero Brockhoff, Anja Pickhard

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
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 5 institutions in 2 countries.

Carlotta SchieflerDepartment of Otolaryngology Head and Neck Surgery, Technical University of Munich, 81675 Muenchen, Germany.
Guido PiontekDepartment of Otolaryngology Head and Neck Surgery, Technical University of Munich, 81675 Muenchen, Germany.
Johannes DoescherDepartment of Otolaryngology Head and Neck Surgery, Technical University of Munich, 81675 Muenchen, Germany.
Dominik SchuettlerDepartment of Otolaryngology Head and Neck Surgery, Technical University of Munich, 81675 Muenchen, Germany.
Martin MißlbeckDepartment of Radiotherapy, Technical University of Munich, 81675 Muenchen, Germany.
Martina RudeliusInstitute of Pathology, Julius-Maximilians-University and Comprehensive Cancer Center Mainfranken, Josef-Schneider-Straße 2, 97080 Wuerzburg, Germany.
Anna HaugDepartment of Otolaryngology, University of Innsbruck, Anichstr. 35, 6020 Innsbruck, Austria.
Rudolf ReiterDepartment of Otolaryngology Head and Neck Surgery, Section of Phoniatrics and Pedaudiology, University of Ulm, Prittwitzstr. 43, 89075 Ulm, Germany.
Gero BrockhoffDepartment of Gynecology and Obstetrics, University of Regensburg, 93053 Regensburg, Germany.
Anja PickhardDepartment of Otolaryngology Head and Neck Surgery, Technical University of Munich, 81675 Muenchen, Germany.
Technical University of Munich · DEComprehensive Cancer Center Mainfranken · DEUniversität Innsbruck · ATUniversität Ulm · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SphK1 is known to play a role in tumor progression, resistance to radiochemotherapy, and migration patterns. As the overall survival rates of squamous cell carcinoma of the head and neck (HNSCC) remain poor due to limitations in surgery and irradiation and chemotherapy resistance, SphK1 is an important enzyme to investigate. The purpose of this study was to elucidate the impact of SphK1 on irradiation efficacy of HNSCC in-vitro with emphasis on EGFR signaling. By immunhistochemical staining we found a positive correlation between EGFR and SphK1 expression in patient specimens. In colony formation assays irradiation sensitive cell lines showed a poor response to cetuximab, an EGFR inhibitor, and SKI-II, a SphK1 inhibitor, and vice versa. In irradiation sensitive cells an enhanced reduction of cell migration and survival was found upon simultaneous targeting of EGFR and SphK1. In the present study, we elucidated a linkage between the two signaling pathways with regard to the efficacy of cetuximab treatment and the impact on the migration behavior of tumor cells. We investigated the biological impact of inhibiting these pathways and examined the biochemical implications after different treatments. An understanding of the processes involved could help to improve the treatment of patients with HNSCC.

Indexed as

AgedAged, 80 and overAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCarcinoma, Squamous CellCell Line, TumorCell MovementCetuximabDisease ProgressionErbB ReceptorsFemaleHead and Neck NeoplasmsHumansMaleMiddle AgedParaffin Embedding4-(4-(4-chloro-phenyl)thiazol-2-ylamino)phenolAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabEGFR protein, humanErbB ReceptorsPhosphotransferases (Alcohol Group Acceptor)Sphingosine KinaseThiazoles

Identifiers

PMID25245676
PMCPMC4259444
OpenAlexW1903839759

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.