Drug resistance mechanism and new therapy strategy progression in targeted treatment of gastrointestinal stromal tumors.
- Author:
Yinan SHI
1
;
Xiaobo LIANG
Author Information
1. Department of Minimally Invasive Surgery, Shanxi Tumor Hospital, Taiyuan 030013, China. liangxiaobo@medmail.com.cn.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
Benzamides;
Disease Progression;
Drug Resistance, Neoplasm;
Gastrointestinal Neoplasms;
genetics;
therapy;
Gastrointestinal Stromal Tumors;
genetics;
therapy;
Humans;
Imatinib Mesylate;
Indoles;
Mutation;
Piperazines;
Proto-Oncogene Proteins c-kit;
Pyrimidines;
Pyrroles;
Quality of Life;
Receptor, Platelet-Derived Growth Factor alpha
- From:
Chinese Journal of Gastrointestinal Surgery
2014;17(4):321-325
- CountryChina
- Language:Chinese
-
Abstract:
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 receptor α (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.
