胃肠间质瘤靶向治疗耐药机制及治疗策略新进展
Drug resistance mechanism and new therapy strategy progression in targeted treatment of gastrointestinal stromal tumors
胃肠间质瘤是胃肠道最常见的间叶组织来源肿瘤,获功能性突变的KIT和PDGFRA受体酪氨酸激酶异常活化是多数胃肠间质瘤发病的关键因素。伊马替尼和舒尼替尼等分子靶向药物是晚期或不可切除胃肠间质瘤患者疗效确切的一线及二线治疗选择,但伊马替尼耐药是临床中的棘手问题及研究热点。本文对伊马替尼耐药的分子机制和耐药后治疗策略的选择以及靶向治疗的新进展进行讨论。未来分子生物学指导下的个体化治疗有望进一步提高胃肠间质瘤疗效,改善患者生存。
更多Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the gastrointestinal tract. Most of these stromal tumors are characterized by mutations in the KTT or platelet-derived growth factor receptorα (PDGFRA) genes, resulting in the constitutive activation of tyrosine kinase signaling. Tyrosine kinase inhibitors (TKI), such as imatinib and sunitinib, provide the standard first-line and second-line therapy for patients with metastatic or unresectable GIST. Imatinib resistance has been a challenging problem in clinical practice and raised great concern. This review introduces the underlying mechanisms of imatinib resistance and advances of treatment strategies. Reasonable individual treatment with the guidance of molecular biology is promising to improve the efficacy and the quality of life for GIST patients.
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