Simpson Laboratory, The University of Queensland Diamantina Institute, Woolloongabba, Brisbane 4102, Australia.
Department of General Surgery, Mater Hospital Brisbane, South Brisbane 4101, Australia.
Cells. 2021 May 14;10(5):1206. doi: 10.3390/cells10051206.
Globally, lung cancer is the leading cause of cancer-related death. The majority of non-small cell lung cancer (NSCLC) tumours express epidermal growth factor receptor (EGFR), which allows for precise and targeted therapy in these patients. The dysregulation of EGFR in solid epithelial cancers has two distinct mechanisms: either a kinase-activating mutation in EGFR (EGFR-mutant) and/or an overexpression of wild-type EGFR (wt-EGFR). The underlying mechanism of EGFR dysregulation influences the efficacy of anti-EGFR therapy as well as the nature of resistance patterns and secondary mutations. This review will critically analyse the mechanisms of EGFR expression in NSCLC, its relevance to currently approved targeted treatment options, and the complex nature of secondary mutations and intrinsic and acquired resistance patterns in NSCLC.
在全球范围内，肺癌是癌症相关死亡的主要原因。大多数非小细胞肺癌 (NSCLC) 肿瘤表达表皮生长因子受体 (EGFR)，这使得这些患者能够进行精确和靶向治疗。固体上皮癌中 EGFR 的失调有两种不同的机制：EGFR 中的激酶激活突变 (EGFR-突变) 和/或野生型 EGFR 的过度表达 (wt-EGFR)。EGFR 失调的潜在机制影响抗 EGFR 治疗的疗效以及耐药模式和继发性突变的性质。本综述将批判性地分析 NSCLC 中 EGFR 表达的机制、其与目前批准的靶向治疗选择的相关性，以及 NSCLC 中继发性突变和内在及获得性耐药模式的复杂性。
