Evidence map›Paper›PMID 23401458›Full record

ReviewJournal of clinical oncology : official journal of the American Society of Clinical Oncology2013

MET as a possible target for non-small-cell lung cancer.

Ahad A Sadiq, Ravi Salgia

Abstract readReview
In one paragraph

Review in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 2 pooled it
12.0field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Predictive effect of XRCC3 Thr241Met polymorphism on platinum-based chemotherapy in lung cancer patients: meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Article
  8. MET and SLFN11 as a Players in the SCLC Molecular Subtyping Game.International journal of molecular sciences · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

36 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

2 authors at 1 institution in 1 country.

Ahad A SadiqUniversity of Chicago, Chicago, IL, USA.
Ravi Salgia
University of Illinois Chicago · US

Funding

Role of c-Met in SCLC and Potential for Novel TherapyR01CA100750 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2004 to 2012
$2.2M
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
NCI NIH HHS 5R01 CA100750-09NCI NIH HHS 5R01CA125541-05NCI NIH HHS R01 CA100750NCI NIH HHS R01 CA125541
6 · The paper itself

Abstract

Lung cancer is a heterogeneous group of disorders that is now being subdivided into molecular subtypes with dedicated targeted therapies. The MET receptor tyrosine kinase has been identified as aberrantly overexpressed, potentially having activating mutations, and amplified in certain subsets of lung cancers. The ligand hepatocyte growth factor (HGF) can also be overexpressed in lung cancer or expressed in stroma, and both the MET receptor and the HGF ligand can be targets for therapeutics, especially in lung cancer. Activation of MET leads to a plethora of biochemical and biologic changes both in normal and cancerous cells. Preclinically, it has been shown that silencing or inactivating MET leads to decreased viability of cancer cells. There are a number of compounds against MET/HGF in clinical trials that have been shown to be active in lung cancers. This review will summarize the biology of MET as well as its therapeutic inhibition in lung cancer.

Indexed as

Antineoplastic AgentsBiomarkers, TumorCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansLung NeoplasmsMutationProto-Oncogene Proteins c-metAntineoplastic AgentsBiomarkers, TumorHepatocyte Growth FactorProto-Oncogene Proteins c-met

Identifiers

PMID23401458
PMCPMC3589702
OpenAlexW2101441514

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.