Evidence map›Paper›PMID 32888330›Full record

ReviewCancer2020

The METeoric rise of MET in lung cancer.

Alex Friedlaender, Alexander Drilon, Giuseppe Luigi Banna, Solange Peters, Alfredo Addeo

Open access · greenAbstract readReview
In one paragraph

Review in Cancer, 2020. 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
3.4field-weighted citation impact, top 6% 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, 49 citations in OpenAlex.

  1. Trial
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  10. Review
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  12. The MET Oncogene: An Update on Targeting Strategies.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
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  14. Article
  15. Article
  16. Review
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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

5 authors at 4 institutions in 3 countries.

Alex FriedlaenderDepartment of Oncology, University Hospital of Geneva, Geneva, Switzerland.ORCID 0000-0003-1956-6824
Alexander DrilonThoracic Oncology Service, Division of Solid Tumor Oncology, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID 0000-0001-6806-9061
Giuseppe Luigi BannaOncology Department, Portsmouth Hospitals NHS Trust, Portsmouth, United Kingdom.ORCID 0000-0003-0764-3650
Solange PetersOncology Department, Vaudois University Medical Center, Lausanne University, Lausanne, Switzerland.ORCID 0000-0002-0412-7143
Alfredo AddeoDepartment of Oncology, University Hospital of Geneva, Geneva, Switzerland.ORCID 0000-0003-0988-0828
University Hospital of Geneva · CHMemorial Sloan Kettering Cancer Center · USPortsmouth Hospitals NHS Trust · GBUniversity of Lausanne · CH

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Elisa de Stanchina · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Over the years, there has been a continuous increase in clinically relevant driver mutations in patients with non-small cell lung cancer (NSCLC). Among these, dysregulated activation of the MET tyrosine kinase receptor has gained importance due to the recent development of quite effective treatments. MET dysregulation encompasses a heterogeneous array of alterations leading to the prolonged activation of the cellular MET (c-MET or MET) receptor and downstream proliferation pathways. It can arise through several mechanisms, including gene amplification, overexpression of the receptor and/or its ligand hepatocyte growth factor, and the acquisition of activating mutations. MET mutations are found in approximately 3% to 5% of patients with NSCLC, mainly adenocarcinoma, and are overrepresented in the sarcomatoid subtype. De novo MET amplifications are found in 1% to 5% of NSCLC cases, also predominantly in adenocarcinoma. In the current review, the authors discussed the biology of MET, how to diagnose clinically relevant alterations, and the rising clinical importance of these alterations in light of the emergence of multiple targeted therapies, both within the context of MET as a driver of resistance and in its own right.

Indexed as

Carcinoma, Non-Small-Cell LungClinical Trials, Phase I as TopicClinical Trials, Phase II as TopicHumansLung NeoplasmsProto-Oncogene Proteins c-metRetrospective StudiesMET protein, humanProto-Oncogene Proteins c-metMETmolecular oncologynon-small cell lung cancer (NSCLC)precision medicinetargeted therapy

Identifiers

PMID32888330
PMCPMC9066984
OpenAlexW3083007885

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.