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Updated: May 25, 2026

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
Published on: July 25, 2020
Targeting MET in cancer: rationale and progress
Ermanno Gherardi1, Walter Birchmeier, Carmen Birchmeier
1Medical Research Council (MRC) Centre, Hills Road, Cambridge CB2 2QH, UK. egherard@mrc-lmb.cam.ac.uk
Abstract:
Uncontrolled cell survival, growth, angiogenesis and metastasis are essential hallmarks of cancer. Genetic and biochemical data have demonstrated that the growth and motility factor hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, the tyrosine kinase MET, have a causal role in all of these processes, thus providing a strong rationale for targeting these molecules in cancer. Parallel progress in understanding the structure and function of HGF/SF, MET and associated signalling components has led to the successful development of blocking antibodies and a large number of small-molecule MET kinase inhibitors. In this Review, we discuss these advances, as well as results from recent clinical studies that demonstrate that inhibiting MET signalling in several types of solid human tumours has major therapeutic value.
Insights
Targeting the hepatocyte growth factor/scatter factor (HGF/SF) and its receptor MET pathway shows significant therapeutic potential in treating solid human tumors. Advances in understanding this pathway have led to effective inhibitors for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Uncontrolled cell survival, growth, angiogenesis, and metastasis are key cancer hallmarks.
- Hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, MET, play crucial roles in these cancer processes.
- Targeting the HGF/SF-MET pathway is a validated strategy in cancer therapy.
Purpose of the Study:
- To review advances in understanding the HGF/SF-MET signaling pathway.
- To discuss the development and efficacy of MET inhibitors in cancer treatment.
- To highlight the therapeutic value of targeting MET in solid tumors.
Main Methods:
- Review of genetic and biochemical data.
- Analysis of structural and functional studies of HGF/SF, MET, and signaling components.
- Examination of recent clinical trial results for MET inhibitors.
Main Results:
- HGF/SF and MET are causally linked to cancer hallmarks.
- Development of effective blocking antibodies and small-molecule MET kinase inhibitors.
- Clinical studies demonstrate significant therapeutic value of MET inhibition in various solid tumors.
Conclusions:
- Inhibiting the MET signaling pathway offers major therapeutic benefits for human solid tumors.
- Continued research and development of MET-targeted therapies hold promise for cancer treatment.
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