Evidence map›Paper›PMID 20360610›Full record

ArticleThe Journal of biological chemistry2010

EphA2 mutation in lung squamous cell carcinoma promotes increased cell survival, cell invasion, focal adhesions, and mammalian target of rapamycin activation.

Leonardo Faoro, Patrick A Singleton, Gustavo M Cervantes, Frances E Lennon, Nicholas W Choong, Rajani Kanteti, Benjamin D Ferguson, Aliya N Husain, Maria S Tretiakova, Nithya Ramnath and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
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  4. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
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  10. Review
  11. Article
  12. Review
  13. Cortactin in Lung Cell Function and Disease.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

15 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

Leonardo FaoroSection of Hematology and Oncology, Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Patrick A Singleton
Gustavo M Cervantes
Frances E Lennon
Nicholas W Choong
Rajani Kanteti
Benjamin D Ferguson
Aliya N Husain
Maria S Tretiakova
Nithya Ramnath
Everett E Vokes
Ravi Salgia
University of Chicago · USUniversity of Michigan–Ann Arbor · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAL, RATNESHWAR · 1998 to 2012
$27.8M
Role of c-Met in SCLC and Potential for Novel TherapyR01CA100750 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2004 to 2012
$2.2M
Role of Paxillin in Lung CancerR01CA129501 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2008 to 2012
$1.8M
Studies of a Novel Therapeutic Target in Non-Small Cell Lung Cancer (NSCLC)R01CA125541 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2007 to 2011
$1.4M
Novel Targeted Therapy in Pancreatic CancerR21CA140003 · NCI · UNIVERSITY OF CHICAGO · PI KINDLER, HEDY L, SALGIA, RAVI · 2009 to 2010
$378k
NCI NIH HHS 3R01CA100750-06S1NCI NIH HHS 5R01CA100750-07NCI NIH HHS 5R01CA125541-04NCI NIH HHS 5R01CA129501-02NCI NIH HHS 5R21CA140003-02NCI NIH HHS R01 CA100750NCI NIH HHS R01 CA125541NCI NIH HHS R01 CA129501NCI NIH HHS R21 CA140003NHLBI NIH HHS 5P01HL058064-140009
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) has a poor prognosis and improved therapies are needed. Expression of EphA2 is increased in NSCLC metastases. In this study, we investigated EphA2 mutations in NSCLC and examined molecular pathways involved in NSCLC. Tumor and cell line DNA was sequenced. One EphA2 mutation was modeled by expression in BEAS2B cells, and functional and biochemical studies were conducted. A G391R mutation was detected in H2170 and 2/28 squamous cell carcinoma patient samples. EphA2 G391R caused constitutive activation of EphA2 with increased phosphorylation of Src, cortactin, and p130(Cas). Wild-type (WT) and G391R cells had 20 and 40% increased invasiveness; this was attenuated with knockdown of Src, cortactin, or p130(Cas). WT and G391R cells demonstrated a 70% increase in focal adhesion area. Mammalian target of rapamycin (mTOR) phosphorylation was increased in G391R cells with increased survival (55%) compared with WT (30%) and had increased sensitivity to rapamycin. A recurrent EphA2 mutation is present in lung squamous cell carcinoma and increases tumor invasion and survival through activation of focal adhesions and actin cytoskeletal regulatory proteins as well as mTOR. Further study of EphA2 as a therapeutic target is warranted.

Indexed as

Gene Expression Regulation, NeoplasticMutationCarcinoma, Squamous CellCell Line, TumorCell SurvivalDNA Mutational AnalysisFocal AdhesionsHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsLung NeoplasmsNeoplasm InvasivenessOligonucleotide Array Sequence AnalysisProtein Serine-Threonine KinasesReceptor, EphA2TOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsMTOR protein, humanProtein Serine-Threonine KinasesReceptor, EphA2TOR Serine-Threonine Kinases

Identifiers

PMID20360610
PMCPMC2881783
OpenAlexW1536223993

What OpenQuestion holds

Textmetadata
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.