ALK rearrangement in non-small cell lung cancer

被引:0
|
作者
Naulleau, Gaspard [1 ]
Birsen, Gary [1 ]
Mansuet-Lupo, Audrey [2 ,3 ]
Leroy, Karen [4 ]
Wislez, Marie [1 ,3 ]
机构
[1] Univ Paris Cite, Hop Cochin, AP HP Ctr, Serv Pneumol, Paris, France
[2] Univ Paris Cite, Hop Cochin, AP HP Ctr, Serv Anat Pathol, Paris, France
[3] Univ Paris Cite, Ctr Rech Cordeliers, Equipe Inflammat Complement & Canc, INSERM,U1138, Paris, France
[4] Univ Paris Cite, Hop Europeen Georges Pompidou, AP HP Ctr, Serv Biochim, Paris, France
关键词
ALK rearrangement; Targeted therapy; Non-small cell lung carcinoma; Resistance mechanisms; GENERATION SEQUENCING REVEALS; RECEPTOR TYROSINE KINASE; EML4-ALK FUSION GENE; HISTOLOGICAL TRANSFORMATION; NSCLC PATIENTS; RESISTANCE; ADENOCARCINOMA; CRIZOTINIB; MUTATION; ALECTINIB;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The discovery of ALK gene rearrangement in 3 to 5% of non-small cell lung carcinomas has revolutionized our understanding and therapeutic approach of these cancers. This oncogenic driver is associated with specific clinical and biological features is associated with specific clinical and biological features, mainly affecting young and never-smoker patients, with a particular tropism outcomes, with remarkable efficacy of latest-generation molecules, particularly in controlling brain metastases. However, the emergence of complex resistance mechanisms, whether ALK-dependent or ALK-independent, remains a major challenge. The comprehensive understanding of these resistance mechanisms now guides the development of next-generation inhibitors and innovative therapeutic strategies, paving the way for increasingly personalized precision medicine.
引用
收藏
页码:3S86 / 3S94
页数:9
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