Overcoming therapy resistance in EGFR-mutant lung cancer

被引:388
作者
Passaro, Antonio [1 ]
Janne, Pasi A. [2 ,3 ]
Mok, Tony [4 ]
Peters, Solange [5 ]
机构
[1] IRCCS, European Inst Oncol, Div Thorac Oncol, Milan, Italy
[2] Dana Farber Canc Inst, Lowe Ctr Thorac Oncol, Boston, MA 02115 USA
[3] Harvard Med Sch, Boston, MA 02115 USA
[4] Chinese Univ Hong Kong, Dept Clin Oncol, State Key Lab Translat Oncol, Hong Kong, Peoples R China
[5] Ctr Hosp Univ Vaudois CHUV, Dept Oncol, Lausanne, Switzerland
关键词
GROWTH-FACTOR RECEPTOR; CIRCULATING TUMOR DNA; CISPLATIN PLUS GEMCITABINE; PHASE-III TRIAL; CELL-FREE DNA; OPEN-LABEL; BRAIN METASTASES; DRUG-RESISTANCE; T790M MUTATION; 1ST-LINE TREATMENT;
D O I
10.1038/s43018-021-00195-8
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tyrosine kinase inhibitors (TKIs) have dramatically changed the clinical prospects of patients with non-small cell lung cancer harboring epidermal growth factor receptor (EGFR)-activating mutations. Despite prolonged disease control and high tumor response rates, all patients eventually progress on EGFR TKI treatment. Here, we review the mechanisms of acquired EGFR TKI resistance, the methods for monitoring its appearance, as well as current and future efforts to define treatment strategies to overcome resistance. Passaro and colleagues discuss recent advances in treating EGFR-mutant lung cancer, including methods for detecting disease and tracking therapy response, developments in understanding of resistance mechanisms and ongoing clinical trials to circumvent therapeutic resistance to EGFR targeting.
引用
收藏
页码:377 / 391
页数:15
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