Evidence map›Paper›PMID 23844053›Full record

ArticlePloS one2013

The EphB4 receptor tyrosine kinase promotes lung cancer growth: a potential novel therapeutic target.

Benjamin D Ferguson, Ren Liu, Cleo E Rolle, Yi-Hung Carol Tan, Valery Krasnoperov, Rajani Kanteti, Maria S Tretiakova, Gustavo M Cervantes, Rifat Hasina, Robyn D Hseu and 8 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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Article
  3. CAR-T cell immunotherapy in rhabdomyosarcoma.Journal of translational medicine · 2026
    Review
  4. Article
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. May EPH/Ephrin Targeting Revolutionize Lung Cancer Treatment?International journal of molecular sciences · 2022
    Review
  12. The role of EphA7 in different tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

18 authors at 4 institutions in 1 country.

Benjamin D FergusonPritzker School of Medicine, University of Chicago, Chicago, Illinois, USA.
Ren Liu
Cleo E Rolle
Yi-Hung Carol Tan
Valery Krasnoperov
Rajani Kanteti
Maria S Tretiakova
Gustavo M Cervantes
Rifat Hasina
Robyn D Hseu
A John Iafrate
Theodore Karrison
Mark K Ferguson
Aliya N Husain
Leonardo Faoro
Everett E Vokes
Parkash S Gill
Ravi Salgia
University of Chicago · USVasGene Therapeutics (United States) · USMassachusetts General Hospital · USUniversity of Southern California · US

Funding

Role of Paxillin in Lung CancerR01CA129501 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2008 to 2012
$1.8M
NCI NIH HHS R01 CA129501NCI NIH HHS R01 CA 129501 05NICHD NIH HHS T32HD009007
6 · The paper itself

Abstract

Despite progress in locoregional and systemic therapies, patient survival from lung cancer remains a challenge. Receptor tyrosine kinases are frequently implicated in lung cancer pathogenesis, and some tyrosine kinase inhibition strategies have been effective clinically. The EphB4 receptor tyrosine kinase has recently emerged as a potential target in several other cancers. We sought to systematically study the role of EphB4 in lung cancer. Here, we demonstrate that EphB4 is overexpressed 3-fold in lung tumors compared to paired normal tissues and frequently exhibits gene copy number increases in lung cancer. We also show that overexpression of EphB4 promotes cellular proliferation, colony formation, and motility, while EphB4 inhibition reduces cellular viability in vitro, halts the growth of established tumors in mouse xenograft models when used as a single-target strategy, and causes near-complete regression of established tumors when used in combination with paclitaxel. Taken together, these data suggest an important role for EphB4 as a potential novel therapeutic target in lung cancer. Clinical trials investigating the efficacy of anti-EphB4 therapies as well as combination therapy involving EphB4 inhibition may be warranted.

Indexed as

AnimalsAntineoplastic AgentsAutopsyCarcinomaCell Line, TumorCell MovementCell ProliferationCell SurvivalDrug SynergismGene DosageGene ExpressionHumansLung NeoplasmsMicePaclitaxelProtein Kinase InhibitorsAntineoplastic AgentsPaclitaxelProtein Kinase InhibitorsReceptor, EphB4RNA, Small Interfering

Identifiers

PMID23844053
PMCPMC3699624
OpenAlexW2080898465

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.