Abstract
Mutation-activated signaling from the KIT and PDGFRA kinases has been successfully targeted in gastrointestinal stromal tumors (GISTs), with subtle differences between the mutations serving to refine prognosis and more precisely tailor therapy. There is a growing understanding of the molecular drivers of GISTs lacking mutations in KIT or PDGFRA, so called wild-type GISTs, further aiding in management decisions. This article provides an overview of all the known molecular subtypes of GIST and provides information about clinical correlates, treatment, and prognosis depending on the subtype.
Keywords:
GIST; KIT; PDGFRA; RTK-wild-type; SDH.
Published by Elsevier Inc.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Biomarkers, Tumor / genetics
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Biomarkers, Tumor / metabolism
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Drug Resistance, Neoplasm
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Gastrointestinal Neoplasms / classification
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Gastrointestinal Neoplasms / diagnosis*
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Gastrointestinal Neoplasms / drug therapy
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Gastrointestinal Neoplasms / genetics
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Gastrointestinal Stromal Tumors / classification
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Gastrointestinal Stromal Tumors / diagnosis*
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Gastrointestinal Stromal Tumors / drug therapy
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Gastrointestinal Stromal Tumors / genetics
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Humans
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Mutation
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Protein Kinase Inhibitors / pharmacology
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Protein Kinase Inhibitors / therapeutic use
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Signal Transduction
Substances
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Antineoplastic Agents
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Biomarkers, Tumor
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Protein Kinase Inhibitors