Abstract
Gastrointestinal stromal tumors (GISTs) owe their development to the activating mutations in mast/stem cell growth factor receptor (KIT) or platelet-derived growth factor receptor A (PDGFRA) oncogenes. Both these KIT and PDGFRA oncogenes are members of the type III transmembrane receptor tyrosine kinase family that stimulates intracellular signaling pathways controlling cell proliferation, adhesion, apoptosis, survival, and differentiation. The presence and type of KIT/PDGFRA mutations help to predict the imatinib mesylate therapy, a selective tyrosine kinase inhibitor. Moreover, there is reported a small proportion of wild-type GISTs for both KIT and PDGFRA genes, and tumors more often acquire secondary mutations on KIT, that results into imatinib resistance. New patents to the GISTs imatinib resistant have recently been introduced. At present, sunitinib, is prescribed as second line therapy for patients with imatinibresistant or imatinib-intolerant GIST, and a number of other drugs, such as masitinib and valatinib, are in the pipeline. The present research focuses on GISTs diagnostic, prognostic and therapeutic biomarkers and addresses the development of novel patents for the treatment of these patients.
Keywords: Gastrointestinal stromal tumor, imatinib, KIT, new patents, PDGFRA, sunitinib.
Recent Patents on Anti-Cancer Drug Discovery
Title:Biomarkers and Novel Therapeutic Targets in Gastrointestinal Stromal Tumors (GISTs)
Volume: 8 Issue: 3
Author(s): Nathalia C. Campanella, Antonio T. de Oliveira, Cristovam Scapulatempo-Neto, Denise P. Guimaraes and Rui M. Reis
Affiliation:
Keywords: Gastrointestinal stromal tumor, imatinib, KIT, new patents, PDGFRA, sunitinib.
Abstract: Gastrointestinal stromal tumors (GISTs) owe their development to the activating mutations in mast/stem cell growth factor receptor (KIT) or platelet-derived growth factor receptor A (PDGFRA) oncogenes. Both these KIT and PDGFRA oncogenes are members of the type III transmembrane receptor tyrosine kinase family that stimulates intracellular signaling pathways controlling cell proliferation, adhesion, apoptosis, survival, and differentiation. The presence and type of KIT/PDGFRA mutations help to predict the imatinib mesylate therapy, a selective tyrosine kinase inhibitor. Moreover, there is reported a small proportion of wild-type GISTs for both KIT and PDGFRA genes, and tumors more often acquire secondary mutations on KIT, that results into imatinib resistance. New patents to the GISTs imatinib resistant have recently been introduced. At present, sunitinib, is prescribed as second line therapy for patients with imatinibresistant or imatinib-intolerant GIST, and a number of other drugs, such as masitinib and valatinib, are in the pipeline. The present research focuses on GISTs diagnostic, prognostic and therapeutic biomarkers and addresses the development of novel patents for the treatment of these patients.
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Campanella C. Nathalia, Oliveira de Antonio T., Scapulatempo-Neto Cristovam, Guimaraes P. Denise and Reis M. Rui, Biomarkers and Novel Therapeutic Targets in Gastrointestinal Stromal Tumors (GISTs), Recent Patents on Anti-Cancer Drug Discovery 2013; 8 (3) . https://dx.doi.org/10.2174/15748928113089990030
DOI https://dx.doi.org/10.2174/15748928113089990030 |
Print ISSN 1574-8928 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3970 |
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