Treatment modalities for advanced ALK-rearranged non-small-cell lung cancer

被引：14

作者：

Sullivan, Ivana ^{[1
]}

Planchard, David ^{[1
]}

机构：

[1] Inst Gustave Roussy, Med Oncol Dept, 114 Rue Edouard Vaillant, F-94805 Villejuif, France

来源：

FUTURE ONCOLOGY | 2016年 / 12卷 / 07期

关键词：

alectinib; ALK-rearrangement; CNS disease; ceritinib; crizotinib; crizotinib-resistance; non-small-cell lung cancer; EML4-ALK FUSION GENE; LYMPHOMA KINASE ALK; MOLECULAR CHAPERONE HSP90; HIGH-DOSE CRIZOTINIB; BRAIN METASTASES; ACQUIRED-RESISTANCE; OLIGOPROGRESSIVE DISEASE; INHIBITOR ALECTINIB; ANTITUMOR-ACTIVITY; CONFER RESISTANCE;

D O I：

10.2217/fon.16.15

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The ALK gene plays a key role in the pathogenesis of non-small-cell lung cancer (NSCLC). Patients with NSCLC harboring an ALK-rearrangement represent the second oncogene addiction to be identified in this disease. Crizotinib was the first ALK inhibitor showing pronounced clinical activity, and is now a reference treatment for ALK-positive NSCLC disease. However, despite initial impressive responses to crizotinib, acquired resistance almost invariably develops within 12 months. The pressing need for effective second-line agents has prompted the rapid development of next-generation ALK inhibitors. These agents, notably ceritinib and alectinib as the most developed, have a higher potency against ALK than crizotinib, along with activity against tumors harboring crizotinib-resistant mutations and potentially improved CNS penetration.

引用

页码：945 / 961

页数：17

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