Abstract
Tyrosine kinases are frequently deregulated in cancer either by constitutive activation, mutation, or over-expression. Though they are often associated with an aggressive phenotype they are also proving to be a druggable target. Activation of the MET receptor tyrosine kinase promotes cell proliferation, scattering, invasion, survival, and angiogenesis. Deregulation of MET promotes tumor formation, growth, progression, metastasis, and therapeutic resistance. Because MET is a player in so many aspects of cancer development and progression, it is a strong candidate for targeted therapy. Numerous agents have been developed that are able to target MET expression and/or function and are the focus of this review.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Antineoplastic Agents / therapeutic use*
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Cell Proliferation
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Clinical Trials as Topic
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Disease Progression
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Humans
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Medical Oncology / methods
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Models, Biological
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Models, Genetic
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Neoplasm Metastasis
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Neoplasms / drug therapy*
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Neoplasms / metabolism
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Neoplasms / pathology
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Neovascularization, Pathologic
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Oncogenes
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Phenotype
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Protein Structure, Tertiary
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Proto-Oncogene Proteins / antagonists & inhibitors
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Proto-Oncogene Proteins / metabolism*
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Proto-Oncogene Proteins c-met
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Receptors, Growth Factor / antagonists & inhibitors
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Receptors, Growth Factor / metabolism*
Substances
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Antineoplastic Agents
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Proto-Oncogene Proteins
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Receptors, Growth Factor
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MET protein, human
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Proto-Oncogene Proteins c-met