Abstract
Two independent events--the identification of activating mutations of the RET proto-oncogene, a receptor tyrosine kinase, in medullary thyroid carcinoma, and the recognition that small organic molecules could bind to and inhibit phosphorylation of signaling molecules, thereby inactivating the pathway-led to the recognition that kinase inhibitors could be used to treat medullary thyroid carcinoma (MTC). The introduction of these compounds into clinical practice has transformed the treatment of metastatic MTC and provided insight into the mechanisms by which RET causes C-cell transformation. This chapter will review the progress in this field over the past 7 years.
Keywords:
Cabozantinib; Calcitonin; Medullary thyroid carcinoma; Metastasis; Multiple endocrine neoplasia type 2; RET proto-oncogene; Tyrosine kinase inhibitor; Vandetanib.
MeSH terms
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Animals
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Antineoplastic Agents / adverse effects
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Antineoplastic Agents / therapeutic use*
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Carcinoma, Neuroendocrine / drug therapy*
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Carcinoma, Neuroendocrine / enzymology
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Carcinoma, Neuroendocrine / genetics
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Carcinoma, Neuroendocrine / pathology
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Genetic Predisposition to Disease
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Humans
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Molecular Targeted Therapy
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Mutation
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Patient Selection
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Phenotype
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Protein Kinase Inhibitors / adverse effects
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Protein Kinase Inhibitors / therapeutic use*
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Proto-Oncogene Mas
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Proto-Oncogene Proteins c-ret / antagonists & inhibitors*
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Proto-Oncogene Proteins c-ret / genetics
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Proto-Oncogene Proteins c-ret / metabolism
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Risk Factors
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Signal Transduction / drug effects
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Thyroid Neoplasms / drug therapy*
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Thyroid Neoplasms / enzymology
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Thyroid Neoplasms / genetics
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Thyroid Neoplasms / pathology
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Treatment Outcome
Substances
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Antineoplastic Agents
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MAS1 protein, human
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Protein Kinase Inhibitors
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Proto-Oncogene Mas
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Proto-Oncogene Proteins c-ret
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RET protein, human
Supplementary concepts
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Thyroid cancer, medullary