ReviewZhongguo fei ai za zhi = Chinese journal of lung cancer2015
[Mechanism of c-MET in Non-small Cell Lung Cancer and Its Treatment and Testing].
Review in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Junction Plakoglobin - A Dual-Role Player in Cancer Biology.International journal of surgery (London, England) · 2025Review
- Synergistic antitumor activity of low-dose c-Met tyrosine kinase inhibitor and sorafenib on human non-small cell lung cancer cells.Oncology letters · 2018Article
- Overexpression of MicroRNA-27b Inhibits Proliferation, Migration, and Invasion via Suppression of MET Expression.Oncology research · 2017Article
- Expression of HIF-1α and P-gp in non-small cell lung cancer and the relationship with HPV infection.Oncology letters · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocyte growth factor/c-MET (HGF/c-MET) signaling pathway can be abnormal activated by many mechanisms such as c-MET mutation, amplification and the overexpression of HGF, and it plays an important role in the development of non-small cell lung cancer (NSCLC), as well as in the tolerance of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) in NSCLC. Therefore, c-MET is a new molecular target for the therapy of NSCLC since EGFR and ALK. At present, although the c-MET inhibitors have shown a potential prospect in some clinical trials, its assessment of safety and effectiveness in clinical applications, and the choice of testing methods and standards still need a further discussion. In this paper, we summarized the mechanism of c-MET in NSCLC, as well as its treatment prospect and selection of testing methods.
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Identifiers
What OpenQuestion holds
Registered trials
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.