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Acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in EGFR-mutant non-small cell lung cancer: A new era begins
被引:113
|作者:
Remon, J.
[1
]
Moran, T.
[2
]
Majem, M.
[3
]
Reguart, N.
[4
]
Dalmau, E.
[5
]
Marquez-Medina, D.
[6
]
Lianes, P.
[1
]
机构:
[1] Hosp Mataro, Dept Med Oncol, Carretera Cirera S-N, Barcelona 08304, Spain
[2] Univ Autonoma Barcelona, Hosp Germans Trias & Pujol, Inst Catala Oncol Badalona, Dept Med Oncol, Barcelona 08916, Spain
[3] Hosp Santa Creu St & Pau, Dept Med Oncol, Barcelona 08025, Spain
[4] Hosp Clin Barcelona, Dept Med Oncol, E-08036 Barcelona, Spain
[5] Hosp Univ Parc Tuli 1, Dept Med Oncol, Barcelona 08208, Spain
[6] Hosp Arnau Vilanova, Dept Med Oncol, Lleida 25198, Spain
关键词:
Non-small cell lung cancer;
Acquired resistance;
Tyrosine kinase inhibitors;
EGFR-mutant tumors;
EPITHELIAL-MESENCHYMAL TRANSITION;
RANDOMIZED PHASE-II;
MET AMPLIFICATION;
GEFITINIB RESISTANCE;
ERLOTINIB RESISTANCE;
1ST-LINE TREATMENT;
T790M MUTATIONS;
TKI RESISTANCE;
GENE-MUTATIONS;
OPEN-LABEL;
D O I:
10.1016/j.ctrv.2013.06.002
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
The discovery of mutated oncogenes has opened up a new era for the development of more effective treatments for non-small cell lung cancer patients (NSCLC) harbouring EGFR mutations. However, patients with EGFR-activating mutation ultimately develop acquired resistance (AR). Several studies have identified some of the mechanisms involved in the development of AR to EGFR tyrosine kinase inhibitors (TKI) that can be potential therapeutic strategies, although in up to 30% of cases, the underlying mechanism of AR are still unexplained. In this review we aim to summarize the main mechanisms of AR to EGFR TKI and some clinical strategies that can be used in the daily clinical practice to overcome this resistance and try to prolong the outcomes in this subgroup of patients. (C) 2013 Elsevier Ltd. All rights reserved.
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页码:93 / 101
页数:9
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