ALK inhibitors in cancer: mechanisms of resistance and therapeutic management strategies

被引:5
|
作者
Poei, Darin [1 ]
Ali, Sana [2 ]
Ye, Shirley [1 ]
Hsu, Robert [2 ,3 ]
机构
[1] Univ Southern Calif, Dept Internal Med, Los Angeles, CA 90033 USA
[2] Univ Southern Calif, Norris Comprehens Canc Ctr, Div Med Oncol, Los Angeles, CA 90033 USA
[3] Univ Southern Calif, Norris Comprehens Canc Ctr, Dept Med, Div Med Oncol, 1441 Eastlake Ave, Los Angeles, CA 90033 USA
关键词
NSCLC; ALK TKI; acquired resistance; alectinib; crizotinib; lorlatinib; ceritinib; brigatinib; CELL LUNG-CANCER; LYMPHOMA KINASE ALK; GENERATION SEQUENCING REVEALS; PREFERRED 1ST-LINE OPTION; FACTOR RECEPTOR EGFR; OPEN-LABEL; TYROSINE KINASE; PHASE-II; CRIZOTINIB RESISTANCE; ACQUIRED-RESISTANCE;
D O I
10.20517/cdr.2024.25
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Anaplastic lymphoma kinase (ALK) gene rearrangements have been identified as potent oncogenic drivers in several malignancies, including non-small cell lung cancer (NSCLC). The discovery of ALK inhibition using a tyrosine kinase inhibitor (TKI) has dramatically improved the outcomes of patients with ALK-mutated NSCLC. However, the emergence of intrinsic and acquired resistance inevitably occurs with ALK TKI use. This review describes the molecular mechanisms of ALK TKI resistance and discusses management strategies to overcome therapeutic resistance.
引用
收藏
页数:22
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