Abstract
RET is the receptor for glial-derived neurotrophic factor growth factors. It is a paradigm of a single gene that causes different types of human cancer when targeted by different genetic alterations. Like other receptor tyrosine kinases, once activated, RET recruits a variety of signaling molecules that mediate biological responses. Here we review data on the signaling pathways that lead to RET-mediated cell transformation and recent evidence that manipulation of RET holds promise for thyroid cancer treatment.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Carcinoma, Papillary / metabolism
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Cell Transformation, Neoplastic
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Humans
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Ligands
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Models, Biological
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Models, Genetic
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Neoplasms / metabolism*
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Phosphorylation
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Protein Structure, Tertiary
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Proto-Oncogene Proteins / physiology*
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Proto-Oncogene Proteins c-ret
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Receptor Protein-Tyrosine Kinases / physiology*
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Signal Transduction
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Thyroid Neoplasms / metabolism
Substances
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Ligands
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-ret
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Receptor Protein-Tyrosine Kinases