作者: Christopher L. Corless , Michael C. Heinrich
DOI: 10.1146/ANNUREV.PATHMECHDIS.3.121806.151538
关键词: Imatinib mesylate 、 Receptor tyrosine kinase 、 Imatinib 、 Tyrosine-kinase inhibitor 、 Growth factor receptor 、 Biology 、 Tyrosine kinase 、 Pathology 、 Sunitinib 、 Cancer research 、 Stromal cell
摘要: Gastrointestinal stromal tumors (GISTs) form an interesting group of sarcomas whose unique pathobiology provides a model how molecularly targeted therapeutics can have major impact on patient welfare. Approximately 85% GISTs are driven by oncogenic mutations in either two receptor tyrosine kinases: KIT or plateletderived growth factor α. We review the pivotal relationship between specific these kinase genes, origin and pathologic spectrum GISTs, response to treatment with inhibitors such as imatinib sunitinib. Mechanisms resistance inhibitor therapy discussed, targets for next generation considered. The rapid evolution our understanding which stems directly from close alliance basic clinical researchers field, illustrates growing role molecular classification solid development modern oncological treatments.