Acquired resistance of non-small cell lung cancer to epidermal growth factor receptor tyrosine kinase inhibitors

被引：41

作者：

Nurwidya, Fariz ^{[1
]}

Takahashi, Fumiyuki ^{[1
]}

Murakami, Akiko ^{[1
]}

Kobayashi, Isao ^{[1
]}

Kato, Motoyasu ^{[1
]}

Shukuya, Takehito ^{[1
]}

Tajima, Ken ^{[1
]}

Shimada, Naoko ^{[1
]}

Takahashi, Kazuhisa ^{[1
]}

机构：

[1] Juntendo Univ, Grad Sch Med, Dept Resp Med, Bunkyo Ku, Tokyo 1138421, Japan

来源：

RESPIRATORY INVESTIGATION | 2014年 / 52卷 / 02期

关键词：

Acquired resistance; Epidermal growth factor receptor (EGFR); Non-small cell lung cancer (NSCLC); Tyrosine kinase inhibitors;

D O I：

10.1016/j.resinv.2013.07.007

中图分类号：

R56 [呼吸系及胸部疾病];

学科分类号：

摘要：

Activation of epidermal growth factor receptor (EGFR) triggers anti-apoptotic signaling, proliferation, angiogenesis, invasion, metastasis, and drug resistance, which leads to development and progression of human epithelial cancers, including non-small cell lung cancer (NSCLC). Inhibition of EGFR by tyrosine kinase inhibitors such as gefitinib and erlotinib has provided a new hope for the cure of NSCLC patients. However, acquired resistance to gefitinib and erlotinib via EGFR-mutant NSCLC has occurred through various molecular mechanisms such as T790M secondary mutation, MET amplification, hepatocyte growth factor (HGF) overexpression, PTEN downregulation, epithelial-mesenchymal transition (EMT), and other mechanisms. This review will discuss the biology of receptor tyrosine kinase inhibition and focus on the molecular mechanisms of acquired resistance to tyrosine kinase inhibitors of EGFR-mutant NSCLC. (C) 2013 The Japanese Respiratory Socity. Published by Elsevier B.V. All rights reserved.

引用

页码：82 / 91

页数：10

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