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Targeting MET in cancer therapy - PMC
Source: ncbi.nlm.nih.gov
Article summary:
1. MET encodes a receptor tyrosine kinase c-MET for hepatocyte growth factor (HGF) which activates downstream signaling pathways to trigger cell migration, proliferation, and angiogenesis.
2. MET exon 14 alterations and MET gene amplification play a critical role in the origin of cancer.
3. Several monoclonal antibodies and small-molecule inhibitors of c-MET have been evaluated in clinical trials with varying results.
Article analysis:
The article is generally reliable and trustworthy as it provides an overview of the current research on targeting MET in cancer therapy. The article is well-referenced and provides evidence for its claims, such as citing studies that have evaluated monoclonal antibodies and small-molecule inhibitors of c-MET in clinical trials. The article also provides an overview of the MET pathway, including its structure, function, and role in cancer development.
However, there are some potential biases that should be noted. For example, the article does not provide any information on possible risks associated with targeting MET in cancer therapy or explore any counterarguments to this approach. Additionally, the article does not present both sides equally; instead it focuses primarily on the potential benefits of targeting MET in cancer therapy without providing an equal amount of information on potential drawbacks or risks associated with this approach.
Topics for further research:
Risks associated with targeting MET in cancer therapy
Counterarguments to targeting MET in cancer therapy
Adverse effects of targeting MET in cancer therapy
Clinical trials evaluating targeting MET in cancer therapy
Potential drawbacks of targeting MET in cancer therapy
Long-term effects of targeting MET in cancer therapy