Evidence map›Paper›PMID 27794501›Full record

ReviewJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2017

Targeting MET in Lung Cancer: Will Expectations Finally Be MET?

Alexander Drilon, Federico Cappuzzo, Sai-Hong Ignatius Ou, D Ross Camidge

Abstract readReview
In one paragraph

Review in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

212 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Vebreltinib for Advanced Non-Small Cell Lung Cancer Harboring c-Met Exon 14 Skipping Mutation: A Multicenter, Single-Arm, Phase II KUNPENG Study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
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152 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

4 authors.

Alexander DrilonMemorial Sloan Kettering Cancer Center, New York, New York. Electronic address: drilona@mskcc.org.
Federico CappuzzoAzienda Unità Sanitaria Locale della Romagna, Ravenna, Italy.
Sai-Hong Ignatius OuChao Family Comprehensive Cancer Center, University of California Irvine School of Medicine, Orange, California.
D Ross CamidgeUniversity of Colorado Cancer Center, Aurora, Colorado.

Funding

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

Abstract

The hepatocyte growth factor receptor (MET) is a potential therapeutic target in a number of cancers, including NSCLC. In NSCLC, MET pathway activation is thought to occur through a diverse set of mechanisms that influence properties affecting cancer cell survival, growth, and invasiveness. Preclinical and clinical evidence suggests a role for MET activation as both a primary oncogenic driver in subsets of lung cancer and as a secondary driver of acquired resistance to targeted therapy in other genomic subsets. In this review, we explore the biology and clinical significance behind MET proto-oncogene receptor tyrosine kinase (MET) exon 14 alterations and MET amplification in NSCLC, the role of MET amplification in the setting of acquired resistance to EGFR tyrosine kinase inhibitor therapy in EGFR-mutant NSCLC, and the history of MET pathway inhibitor drug development in NSCLC, highlighting current strategies that enrich for biomarkers likely to be predictive of response. Whereas previous trials that focused on MET pathway-directed targeted therapy in unselected or MET-overexpressing NSCLC yielded largely negative results, more recent investigations focusing on MET exon 14 alterations and MET amplification have been notable for meaningful clinical responses to MET inhibitor therapy in a substantial proportion of patients.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsHumansLung NeoplasmsProto-Oncogene MasProto-Oncogene Proteins c-metAntineoplastic AgentsMAS1 protein, humanMET protein, humanProto-Oncogene MasProto-Oncogene Proteins c-metcrizotinibMET amplificationMET exon 14 skipping alterationsMET inhibitorMET overexpressionnon-small cell lung cancer

Identifiers

PMID27794501
PMCPMC5603268

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.