Evidence map›Paper›PMID 22807579›Full record

ArticleMolecular cancer therapeutics2012

Global evaluation of Eph receptors and ephrins in lung adenocarcinomas identifies EphA4 as an inhibitor of cell migration and invasion.

Pierre Saintigny, Shaohua Peng, Li Zhang, Banibrata Sen, Ignacio I Wistuba, Scott M Lippman, Luc Girard, John D Minna, John V Heymach, Faye M Johnson

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Eph Receptors in Cancer.Biomedicines · 2023
    Review
  10. Article
  11. Extracellular RNA in melanoma: Advances, challenges, and opportunities.Frontiers in cell and developmental biology · 2023
    Review
  12. May EPH/Ephrin Targeting Revolutionize Lung Cancer Treatment?International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

10 authors at 2 institutions in 1 country.

Pierre SaintignyDepartment of 1Thoracic/Head & Neck Medical Oncology, The University of Texas MD Anderson Cancer Center;5The University of Texas Graduate School of Biomedical Sciences, Houston, TX 77030, USA. psaintig@mdanderson.org
Shaohua Peng
Li Zhang
Banibrata Sen
Ignacio I Wistuba
Scott M Lippman
Luc Girard
John D Minna
John V Heymach
Faye M Johnson
The University of Texas MD Anderson Cancer Center · USThe University of Texas Southwestern Medical Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
NCI NIH HHS CA 16672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS P50CA070907
6 · The paper itself

Abstract

The Eph family of receptors is the largest family of receptor tyrosine kinases, but it remains poorly studied in lung cancer. We aimed to systematically explore the human Eph receptors and their ligands, the ephrins, in lung adenocarcinoma. The prognostic impact of Eph receptor and ephrin gene expression was analyzed using 2 independent cohorts of lung adenocarcinoma. Gene expression profiles in lung adenocarcinoma compared with normal adjacent lung were studied in 3 independent cohorts and in cell lines. Gene expression profiles were validated with quantitative polymerase chain reaction (qPCR) and Western blotting in cell lines. Functional studies to assess the role of Eph receptor A4 (EphA4) were carried out in vitro. The biological effects of EphA4 in lung cancer cell lines were assayed following overexpression and knockdown. Of the 11 Eph receptors and 8 ephrins analyzed, only EphA4 and ephrin A1 gene expression were consistently associated with an improved outcome in patients with lung adenocarcinoma. Expression levels of EphA4 by microarray correlated well with expression levels measured by qPCR and Western blotting. EphA4 overexpression reduced cell migration and invasion but did not affect cell cycle, apoptosis, or drug sensitivity. Surprisingly, EphA4 was expressed at higher levels in cancer compared with non-cancer tissues and cell lines. EphA4 gene expression is associated with an improved outcome in patients with resected lung adenocarcinoma, possibly by affecting cancer cell migration and invasion.

Indexed as

Cell MovementAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsApoptosisCase-Control StudiesCell Line, TumorCell ProliferationCisplatinDisease-Free SurvivalEphrinsEpithelial CellsErlotinib HydrochlorideExtracellular Signal-Regulated MAP KinasesGene ExpressionHumansAntineoplastic AgentsCisplatinEphrinsErlotinib HydrochlorideExtracellular Signal-Regulated MAP KinasesOccludinOCLN protein, humanQuinazolinesReceptor, EphA4

Identifiers

PMID22807579
PMCPMC3438283
OpenAlexW2132097639

What OpenQuestion holds

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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.