Peter MacCallum Cancer Centre, Melbourne, Vic, Australia.
Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.
Nat Commun. 2024 Feb 28;15(1):1823. doi: 10.1038/s41467-024-46008-1.
In this phase II, single arm trial (ACTRN12617000720314), we investigate if alternating osimertinib and gefitinib would delay the development of resistance to osimertinib in advanced, non-small cell lung cancer (NSCLC) with the epidermal growth factor receptor (EGFR) T790M mutation (n = 47) by modulating selective pressure on resistant clones. The primary endpoint is progression free-survival (PFS) rate at 12 months, and secondary endpoints include: feasibility of alternating therapy, overall response rate (ORR), overall survival (OS), and safety. The 12-month PFS rate is 38% (95% CI 27.5-55), not meeting the pre-specified primary endpoint. Serial circulating tumor DNA (ctDNA) analysis reveals decrease and clearance of the original activating EGFR and EGFR-T790M mutations which are prognostic of clinical outcomes. In 73% of participants, loss of T790M ctDNA is observed at progression and no participants have evidence of the EGFR C797S resistance mutation following the alternating regimen. These findings highlight the challenges of treatment strategies designed to modulate clonal evolution and the clinical importance of resistance mechanisms beyond suppression of selected genetic mutations in driving therapeutic escape to highly potent targeted therapies.
在这项 II 期、单臂试验(ACTRN12617000720314)中,我们研究了在具有表皮生长因子受体(EGFR)T790M 突变的晚期非小细胞肺癌(NSCLC)患者中,交替使用奥希替尼和吉非替尼是否通过调节耐药克隆的选择压力来延迟对奥希替尼的耐药性发展(n=47)。主要终点是 12 个月时无进展生存期(PFS)率,次要终点包括:交替治疗的可行性、总缓解率(ORR)、总生存期(OS)和安全性。12 个月的 PFS 率为 38%(95%CI 27.5-55),未达到预设的主要终点。连续循环肿瘤 DNA(ctDNA)分析显示,原始激活的 EGFR 和 EGFR-T790M 突变减少和清除,这与临床结局相关。在 73%的参与者中,在进展时观察到 T790M ctDNA 的丢失,并且在交替治疗方案后没有参与者存在 EGFR C797S 耐药突变的证据。这些发现强调了旨在调节克隆进化的治疗策略所面临的挑战,以及除了抑制选定的基因突变外,耐药机制在驱动对高度有效的靶向治疗的治疗逃逸方面的临床重要性。