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gastrointestinal stromal tumors/tyrosine
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Optimizing tyrosine kinase inhibitor therapy in gastrointestinal stromal tumors: exploring the benefits of continuous kinase suppression.
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The oral tyrosine kinase inhibitor (TKI) imatinib has revolutionized the treatment of gastrointestinal stromal tumors (GISTs), most of which harbor oncogenic mutation in genes that encode the receptor tyrosine kinases KIT or PDGFA. Imatinib is the standard of care for patients with advanced GIST and
Current management of patients with gastrointestinal stromal tumor receiving the multitargeted tyrosine kinase inhibitor sunitinib.
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BACKGROUND
Gastrointestinal stromal tumor (GIST), a form of soft tissue sarcoma, is often detected incidentally or at an advanced stage. The tyrosine kinase inhibitor sunitinib malate (Sutent * ) is established as second-line treatment for the management of GIST after disease progression on, or
[Molecular mechanism and therapeutic strategy for resistance to tyrosine kinase inhibitors in targeted treatment of gastrointestinal stromal tumors].
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Gastrointestinal stromal tumor (GIST) is the most common mesenchymal neoplasm of the GI tract. Aberrant activation of tyrosine kinase through mutated KIT or platelet-derived growth factor receptor (PDGFRA) is the key pathogenic factor in most cases. Tyrosine kinase inhibitors (TKI) such as imatinib
Activated Tyrosine Kinases in Gastrointestinal Stromal Tumor with Loss of KIT Oncoprotein Expression.
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Oncogenic KIT or PDGFRA receptor tyrosine kinase (TK) mutations are compelling therapeutic targets in gastrointestinal stromal tumors (GISTs), and the KIT/PDGFRA kinase inhibitor, imatinib, is the standard of care for patients with metastatic GIST. However, approximately 10% of KIT-positive GIST
Gain-of-Function Mutations of Receptor Tyrosine Kinases in Gastrointestinal Stromal Tumors.
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Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors in human gastrointestinal tract. We first found that most GISTs expressed KIT, a receptor tyrosine kinase encoded by protooncogene c-kit and that approximately 90% of the sporadic GISTs had somatic gain-of-function
Sunitinib, a multitargeted tyrosine kinase inhibitor, in the management of gastrointestinal stromal tumor.
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Due to the remarkable advances in the understanding of the biology of gastrointestinal stromal tumors (GIST), tyrosine kinase inhibition has become the mainstay of therapy for patients with advanced GIST. Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT,
Differential properties of current tyrosine kinase inhibitors in gastrointestinal stromal tumors.
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During the past decade, tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of gastrointestinal stromal tumors (GIST), providing new treatment options with unprecedented clinical benefit. Recognition of the key role played by the receptor tyrosine kinases KIT and platelet-derived
Management of tyrosine kinase inhibitor-resistant gastrointestinal stromal tumors.
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The treatment of gastrointestinal stromal tumors (GISTs) has been a model for targeted cancer therapy. The discovery of driver somatic mutations in the KIT and PDGFRA receptor tyrosine kinases led to a shift of therapy from conventional cytotoxic chemotherapy to inhibitors of these receptors.
Understanding rechallenge and resistance in the tyrosine kinase inhibitor era: imatinib in gastrointestinal stromal tumor.
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Disease progression after treatment with a particular therapy, in the traditional view of cancer chemotherapy, indicates resistance to that treatment. However, targeted therapies such as tyrosine kinase inhibitors (TKIs) do not follow these same principles. The purpose of this review is to educate
Establishment and characterization of patient-derived xenograft models of gastrointestinal stromal tumor resistant to standard tyrosine kinase inhibitors.
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Gastrointestinal stromal tumors (GISTs) with KIT or platelet-derived growth factor receptor alpha (PDGFRa) oncogenic driver gene mutations, respond to tyrosine kinase inhibitors (TKIs) including imatinib, sunitinib, and regorafenib. However, most patients develop TKI resistance; therefore, novel
Gastrointestinal Stromal Tumor With Multiple Primary Tyrosine Kinase Mutations-Clinicopathologic and Molecular Characterization.
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A unique cohort of chemo-naive gastrointestinal stromal tumors (GISTs) with double-primary tyrosine kinase mutations was characterized particularly to determine whether coexistent mutations represent a single mutational event. Up to 2013, 4 UK centers reported 9 GISTs with 2 primary tyrosine kinase
[Activating mutations in receptor tyrosine kinases with relevance for treatment of gastrointestinal stromal tumors].
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OBJECTIVE
Receptor tyrosine kinases have been shown to be a challenging target for the treatment of hematologic diseases and solid tumors. One very effective tyrosine kinase inhibitor is imatinib mesylate inhibiting the KIT receptor tyrosine kinase in gastrointestinal stromal tumors (GISTs) which
Management of gastrointestinal stromal tumors in the era of tyrosine kinase inhibitors.
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Gastrointestinal stromal tumors (GIST) represent the most common type of mesenchymal malignancy in the gastrointestinal tract. With the discovery of uncontrolled KIT tyrosine kinase signaling as a critical component in the pathogenesis of this disease, the diagnostic and treatment options for
Pharmacogenetics of tyrosine kinase inhibitors in gastrointestinal stromal tumor and chronic myeloid leukemia.
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BACKGROUND
Gastrointestinal stromal tumors (GIST) and chronic myeloid leukemia (CML) are two tumor types deeply different from each other. Despite the differences, these disorders share treatment with tyrosine kinase inhibitor imatinib. Despite the success of imatinib, the response rates vary among
Effect of a tyrosine kinase inhibitor STI571 in a patient with hepatic metastases from a duodenal gastrointestinal stromal tumor.
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Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors. The molecular etiology is the result of mutations in the c-Kit gene. The mutant c-Kit proteins, which are activated without a stem cell factor, contribute to the tumor development. STI571 selectively inhibits c-Kit,
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