Implications of mutational analysis for the management of patients with gastrointestinal stromal tumors and the application of targeted therapies
- PMID: 20690803
- DOI: 10.3109/07357907.2010.494322
Implications of mutational analysis for the management of patients with gastrointestinal stromal tumors and the application of targeted therapies
Abstract
The receptor tyrosine kinase inhibitors, imatinib and sunitinib, have significantly improved the prognosis for patients with advanced gastrointestinal stromal tumors (GISTs). Most GISTs exhibit mutations in the genes encoding the stem cell factor receptor (KIT) or platelet-derived growth factor receptor alpha (PDGFRA). Imatinib is more effective in patients with KIT exon 11 mutations compared with KIT exon 9 mutations and wild-type genotype, while sunitinib confers greater in vitro efficacy in patients with KIT exon 9 mutants and wild-type genotype than in KIT exon 11 mutants. This review examines the potential role of mutational analysis to optimize therapy with imatinib and sunitinib for GIST.
Similar articles
-
[The importance of mutational status in prognosis and therapy of GIST].Recenti Prog Med. 2015 Jan;106(1):17-22. doi: 10.1701/1740.18950. Recenti Prog Med. 2015. PMID: 25621775 Italian.
-
Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumor.J Clin Oncol. 2008 Nov 20;26(33):5352-9. doi: 10.1200/JCO.2007.15.7461. Epub 2008 Oct 27. J Clin Oncol. 2008. PMID: 18955458 Free PMC article. Clinical Trial.
-
The role of KIT in the management of patients with gastrointestinal stromal tumors.Hum Pathol. 2007 May;38(5):679-87. doi: 10.1016/j.humpath.2007.03.001. Hum Pathol. 2007. PMID: 17437861 Review.
-
[Secondary mutation of c-kit/PDGFRα genotypes after imatinib mesylate therapy and its relationship with efficacy of sunitinib].Zhonghua Bing Li Xue Za Zhi. 2012 Jun;41(6):386-90. doi: 10.3760/cma.j.issn.0529-5807.2012.06.006. Zhonghua Bing Li Xue Za Zhi. 2012. PMID: 22932406 Chinese.
-
Correlation of imatinib resistance with the mutational status of KIT and PDGFRA genes in gastrointestinal stromal tumors: a meta-analysis.J Gastrointestin Liver Dis. 2013 Dec;22(4):413-8. J Gastrointestin Liver Dis. 2013. PMID: 24369323 Review.
Cited by
-
Analysis of prognostic factors impacting oncologic outcomes after neoadjuvant tyrosine kinase inhibitor therapy for gastrointestinal stromal tumors.Ann Surg Oncol. 2014 Aug;21(8):2499-505. doi: 10.1245/s10434-014-3632-7. Epub 2014 Mar 18. Ann Surg Oncol. 2014. PMID: 24639192 Free PMC article.
-
Imatinib response of gastrointestinal stromal tumor patients with germline mutation on KIT exon 13: A family report.World J Radiol. 2017 Sep 28;9(9):365-370. doi: 10.4329/wjr.v9.i9.365. World J Radiol. 2017. PMID: 29098070 Free PMC article.
-
Inherited gastrointestinal stromal tumor syndromes: mutations, clinical features, and therapeutic implications.Clin Sarcoma Res. 2012 Oct 4;2(1):16. doi: 10.1186/2045-3329-2-16. Clin Sarcoma Res. 2012. PMID: 23036227 Free PMC article.
-
Durable response with a combination of imatinib and sorafenib in KIT exon 17 mutant gastrointestinal stromal tumor.J Gastrointest Oncol. 2014 Feb;5(1):E27-9. doi: 10.3978/j.issn.2078-6891.2013.058. J Gastrointest Oncol. 2014. PMID: 24490049 Free PMC article.
-
Concurrent Coprimary KIT Exon 17 and BRAF Mutations in a Small Intestinal GI Stromal Tumor-A Case Report.J Gastrointest Cancer. 2025 May 12;56(1):116. doi: 10.1007/s12029-025-01236-6. J Gastrointest Cancer. 2025. PMID: 40353886
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous