التفاصيل البيبلوغرافية
| العنوان: |
Molecular Advances in the Treatment of Advanced Gastrointestinal Stromal Tumor. |
| المؤلفون: |
Venkataraman, Vinayak, George, Suzanne, Cote, Gregory M |
| المصدر: |
Oncologist; Aug2023, Vol. 28 Issue 8, p671-681, 11p, 1 Diagram, 1 Chart |
| مصطلحات موضوعية: |
GASTROINTESTINAL tumors treatment, ONLINE information services, GENETIC mutation, SYSTEMATIC reviews, MOLECULAR pathology, INVESTIGATIONAL drugs, STROMAL cells, PROTEIN-tyrosine kinase inhibitors, MEDLINE, DRUG resistance in cancer cells |
| مستخلص: |
Most gastrointestinal stromal tumors (GIST) are driven by activating mutations in Proto-oncogene c- KIT (KIT) or PDGFRA receptor tyrosine kinases (RTK). The emergence of effective therapies targeting these mutations has revolutionized the management of advanced GIST. However, following initiation of first-line imatinib, a tyrosine kinase inhibitor (TKI), nearly all patients will develop resistance within 2 years through the emergence of secondary resistance mutations in KIT , typically in the Adenosine Triphosphate (ATP)-binding site or activation loop of the kinase domain. Moreover, some patients have de novo resistance to imatinib, such as those with mutations in PDGFRA exon 18 or those without KIT or PDGFRA mutation. To target resistance, research efforts are primarily focused on developing next-generation inhibitors of KIT and/or PDGFRA, which can inhibit alternate receptor conformations or unique mutations, and compounds that impact complimentary pathogenic processes or epigenetic events. Here, we review the literature on the medical management of high-risk localized and advanced GIST and provide an update on clinical trial approaches to this disease. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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