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表皮生长因子受体(EGFR)和 KRAS 基因突变,以及间变性淋巴瘤激酶(ALK)融合:晚期非小细胞肺癌患者的当前进展和个体化治疗。

EGFR and KRAS mutations, and ALK fusions: current developments and personalized therapies for patients with advanced non-small-cell lung cancer.

机构信息

Department of Medical Oncology, Portuguese Oncology Institute, Rua Dr António Bernardino de Almeida, 4200-072, Porto, Portugal.

出版信息

Pharmacogenomics. 2013 Nov;14(14):1765-77. doi: 10.2217/pgs.13.177.

DOI:10.2217/pgs.13.177
PMID:24192124
Abstract

Personalized therapy has significantly developed in lung cancer treatment over recent years. VEGF and EGF play a major role in non-small-cell lung cancer (NSCLC) tumor angiogenesis and aggressiveness. EGFR mutation as well as KRAS and ALK rearrangements are important biomarkers in the field owing to potential targeted therapies involved in clinical practice: erlotinib, geftinib, cetuximab and crizotinib. More recently, regulation of tumor immunity through CTLA4 and PD1/L1 has emerged as a promising field in NSCLC management. This review will focus on the current and future biomarkers in the advanced NSCLC field and also address potential related targeted therapies for these patients.

摘要

近年来,个性化治疗在肺癌治疗中取得了显著进展。VEGF 和 EGF 在非小细胞肺癌(NSCLC)肿瘤血管生成和侵袭性中起主要作用。由于涉及临床实践中的潜在靶向治疗,EGFR 突变以及 KRAS 和 ALK 重排是该领域的重要生物标志物:厄洛替尼、吉非替尼、西妥昔单抗和克唑替尼。最近,通过 CTLA4 和 PD1/L1 调节肿瘤免疫已成为 NSCLC 治疗的一个有前途的领域。本文综述将重点介绍晚期 NSCLC 领域当前和未来的生物标志物,并探讨这些患者潜在的相关靶向治疗。

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