Division of Medical Oncology, Ottawa Hospital Cancer Centre, University of Ottawa, Ottawa, Ontario, Canada.
J Clin Oncol. 2013 Mar 10;31(8):1061-9. doi: 10.1200/JCO.2012.43.4522. Epub 2013 Feb 11.
Worldwide, the majority of patients with advanced non-small-cell lung cancer (NSCLC) do not have activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR). These wild-type patients comprise a significant proportion of those treated with inhibitors of this pathway, and data from randomized trials suggest that some of these wild-type patients will derive a modest benefit from these agents. Although the detection of an activating mutation predicts for a greater likelihood of response and longer progression-free survival from an EGFR tyrosine kinase inhibitor, currently there are no biomarkers that consistently and reproducibly predict for lack of benefit in wild-type patients. Several strategies to increase the efficacy of these inhibitors in wild-type NSCLC are the subject of ongoing investigations.
在全球范围内，大多数晚期非小细胞肺癌（NSCLC）患者的表皮生长因子受体（EGFR）酪氨酸激酶结构域没有激活突变。这些野生型患者占该途径抑制剂治疗的很大一部分，随机试验的数据表明，这些野生型患者中的一些将从这些药物中获得适度的益处。尽管激活突变的检测预测 EGFR 酪氨酸激酶抑制剂的反应可能性更大，无进展生存期更长，但目前没有生物标志物能够一致且可重复地预测野生型患者缺乏获益。正在研究几种增加这些抑制剂在野生型 NSCLC 中的疗效的策略。
