Dowell Jonathan E
Departments of Internal Medicine, University of Texas Southwestern Medical Center, and the Dallas Veterans Affairs Medical Center, Dallas, Texas 75390-8852, USA.
Am J Med Sci. 2006 Mar;331(3):139-49. doi: 10.1097/00000441-200603000-00006.
A large body of preclinical work suggested that the epidermal growth factor receptor (EGFR) would be a successful target for therapy against non-small cell lung cancer (NSCLC), and this led to the development of oral, selective EGFR tyrosine kinase inhibitors (TKI) that improve symptoms and survival in patients with advanced NSCLC. However, not all patients benefit from this treatment, and there has been great interest in identifying the molecular correlates that predict for response to these agents. The recent detection of somatic mutations in EGFR that predict for response to the EGFR tyrosine kinase inhibitors has excited the scientific community. This discovery has far-reaching implications, not only for lung cancer patients treated with an EGFR TKI but also for future drug development in all malignancies.
大量临床前研究表明,表皮生长因子受体(EGFR)将是治疗非小细胞肺癌(NSCLC)的一个成功靶点,这促使了口服、选择性EGFR酪氨酸激酶抑制剂(TKI)的研发,这些抑制剂可改善晚期NSCLC患者的症状并延长生存期。然而,并非所有患者都能从这种治疗中获益,因此人们对确定预测这些药物反应的分子关联因素产生了浓厚兴趣。最近检测到的EGFR体细胞突变可预测对EGFR酪氨酸激酶抑制剂的反应,这一发现引起了科学界的关注。这一发现具有深远意义,不仅对接受EGFR TKI治疗的肺癌患者如此,对所有恶性肿瘤的未来药物研发也是如此。