Evidence map›Paper›PMID 21847116›Full record

ArticleBritish journal of cancer2011

MET phosphorylation predicts poor outcome in small cell lung carcinoma and its inhibition blocks HGF-induced effects in MET mutant cell lines.

E Arriola, I Cañadas, M Arumí-Uría, M Dómine, J A Lopez-Vilariño, O Arpí, M Salido, S Menéndez, E Grande, F R Hirsch and 5 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. MET and SLFN11 as a Players in the SCLC Molecular Subtyping Game.International journal of molecular sciences · 2025
    Article
  4. Article
  5. Article
  6. JTO clinical and research reports · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. ExploitingTranslational lung cancer research · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Targeted drugs in small-cell lung cancer.Translational lung cancer research · 2016
    Review
  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

15 authors at 7 institutions in 2 countries.

E ArriolaOncology Department, Hospital del Mar-Parc de Salut Mar, Passeig Marítim 25-29, 08003, Barcelona, Spain. earriola@hospitaldelmar.cat
I Cañadas
M Arumí-Uría
M Dómine
J A Lopez-Vilariño
O Arpí
M Salido
S Menéndez
E Grande
F R Hirsch
S Serrano
B Bellosillo
F Rojo
A Rovira
J Albanell
Municipal Institute for Medical Research · ESParc de Salut · ESHospital Universitario Fundación Jiménez Díaz · ESHospital Del Mar · ESHospital Universitario Ramón y Cajal · ESPompeu Fabra University · ESUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall cell lung carcinoma (SCLC) has poor prognosis and remains orphan from targeted therapy. MET is activated in several tumour types and may be a promising therapeutic target.

methodsTo evaluate the role of MET in SCLC, MET gene status and protein expression were evaluated in a panel of SCLC cell lines. The MET inhibitor PHA-665752 was used to study effects of pathway inhibition in basal and hepatocyte growth factor (HGF)-stimulated conditions. Immunohistochemistry for MET and p-MET was performed in human SCLC samples and association with outcome was assessed.

resultsIn MET mutant SCLC cells, HGF induced MET phosphorylation, increased proliferation, invasiveness and clonogenic growth. PHA-665752 blocked MET phosphorylation and counteracted HGF-induced effects. In clinical samples, total MET and p-MET overexpression were detected in 54% and 43% SCLC tumours (n = 77), respectively. MET phosphorylation was associated with poor median overall survival (132 days) vs p-MET negative cases (287 days) (P < 0.001). Phospho-MET retained its prognostic value in a multivariate analysis.

conclusionsMET activation resulted in a more aggressive phenotype in MET mutant SCLC cells and its inhibition by PHA-665752 reversed this phenotype. In patients with SCLC, MET activation was associated with worse prognosis, suggesting a role in the adverse clinical behaviour in this disease.

Indexed as

AdultAgedAged, 80 and overCarcinoma, Small CellCell Line, TumorCell ProliferationFemaleHepatocyte Growth FactorHumansIndolesLung NeoplasmsMaleMiddle AgedMutationNeoplasm InvasivenessPhosphorylation5-((2,6-dichlorobenzyl)sulfonyl)-3-((3,5-dimethyl-4-((2-(pyrrolidin-1-ylmethyl)pyrrolidin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-1,3-dihydro-2H-indol-2-oneHepatocyte Growth FactorIndolesProto-Oncogene Proteins c-metSulfones

Identifiers

PMID21847116
PMCPMC3171012
OpenAlexW2158040154

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Registered trials

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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.