ReviewJournal of cellular and molecular medicine2010
Does hepatocyte growth factor/c-Met signal play synergetic role in lung cancer?
Review in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
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Who cites it
5 citing papers in PubMed.
- Article
- Drug combination screening as a translational approach toward an improved drug therapy for chordoma.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition.PloS one · 2017Article
- Gene mutation-based and specific therapies in precision medicine.Journal of cellular and molecular medicine · 2016Article
- Cross-talk between MET and EGFR in non-small cell lung cancer involves miR-27a and Sprouty2.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is growing evidence that the signal pathway between hepatocyte growth factor (HGF) and its receptor c-Met plays an important role in the development of lung cancer, although the specificity of such role is to be clarified. It seems clear that the HGF/c-Met signal contributes to the metastasis of cancer cells to the lung by stimulating the hyperproduction and overactivation of cytokines and enzymes, e.g. HGF, vascular endothelial growth factor and matrix metalloproteases. The HGF/c-Met signal may act as the candidate responsible for the development of epidermal growth factor receptor (EGFR) kinase inhibitor resistance. Experimental evidence showed that the combination of both EGFR and c-Met inhibitors had synergetic or additive therapeutic effects on lung cancer. Although the mechanism of interaction between HGF/c-Met and transforming growth factor-a/EGFR remains unclear, the cross-talk and balance between those two signal pathways are critical and necessary in the development of new therapies for lung cancer.
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Registered trials
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