Research progress on acquired RET fusion induces secondary resistance to EGFR therapy in advanced EGFR-mutated non-small cell lung cancer
10.11855/j.issn.0577-7402.0627.2023.1129
- VernacularTitle:晚期经治非小细胞肺癌EGFR-TKIs获得性RET融合突变耐药的研究进展
- Author:
An WANG
1
;
Tao LI
;
Di LU
;
Yun-Ye MAO
;
Jia-Pei QIN
;
Xin ZHOU
;
Hao FAN
;
Yi HU
Author Information
1. 解放军总医院研究生院/解放军医学院,北京 100853;解放军总医院第一医学中心肿瘤内科,北京 100853
- Keywords:
non-small cell lung cancer;
targeted therapy;
EGFR-TKIs resistance;
rearranged during transfection
- From:
Medical Journal of Chinese People's Liberation Army
2024;49(9):1080-1087
- CountryChina
- Language:Chinese
-
Abstract:
With the in-depth study of molecular biology,non-small cell lung cancer(NSCLC)has opened the era of precision medicine based on mutation-based molecular targeting therapy.Epidermal growth factor receptor(EGFR)driver mutations are closely related to the progression of NSCLC,and EGFR-tyrosine kinase inhibitors(TKIs)developed based on this have achieved significant therapeutic effects,but acquired drug resistance is still one of the major factors limiting their long-term use.As resistance mechanisms are further investigated,in addition to secondary EGFR mutation,MET amplification,HER2 amplification,histologic transformation,etc.,receptor tyrosine kinase(RTK)fusion mutation have been shown to be a targetable mechanism of acquired resistance.Among the acquired RTK fusion mutations,rearranged during transfection(RET)fusion mutations are the accessible targets of our concern.As the RET molecule continues to be explored,drugs targeting RET fusions have been approved and marketed.There are different clinical strategies to deal with acquired RET fusion mutation mediating resistance to EGFR-TKIs treatment.In this review,the structure and function of RET,its relationship with EGFR-TKIs resistance,and treatment strategies are reviewed to further improve patient survival outcomes.
