PDF(Pubmed)
Abstract：
UNASSIGNED: There is a paucity of data on immune checkpoint inhibitors (ICIs) plus doublet chemotherapy (C) in patients with advanced lung cancer whose tumor harbors an actionable mutation. We sought to provide insight into the role of this combination in relation to chemotherapy alone in this patient population.
UNASSIGNED: We conducted a retrospective study at the five University of California National Cancer Institute-designated Comprehensive Cancer Centers. The primary end point was progression-free survival (PFS). Secondary end points included overall survival (OS) and significant adverse events. Adverse events in patients who received a tyrosine kinase inhibitor (TKI) post-ICI were also captured.
UNASSIGNED: A total of 246 patients were identified, 170 treated with C plus ICI and 76 treated with C alone. Driver alterations included EGFR (54.9%), KRAS (32.9%), ALK (5.3%), HER2/ERBB2 (2.9%), ROS1 (1.2%), MET (1.2%), RET (0.8%), and BRAF non-V600 (0.8%). The overall PFS and OS hazard ratios were not significant at 1.12 (95% confidence interval 0.83-1.51; p = 0.472) and 0.86 (95% confidence interval: 0.60-1.24, p = 0.429), respectively. No significant differences in PFS or OS were observed in the mutational subgroups. Grade 3 or greater adverse events were lower in the C plus ICI group. The multivariate analysis for PFS and OS revealed a performance status (Eastern Cooperative Oncology Group) score of 2, and previous TKI treatment was associated with poorer outcomes with C plus ICI.
UNASSIGNED: Our study suggests that patients with oncogenic-driven NSCLC, primarily those with EGFR-driven tumors, treated with a TKI should not subsequently receive C plus ICI. Analysis from prospective clinical trials will provide additional information on the role of ICIs in this group of patients.
UNASSIGNED: We conducted a retrospective study at the five University of California National Cancer Institute-designated Comprehensive Cancer Centers. The primary end point was progression-free survival (PFS). Secondary end points included overall survival (OS) and significant adverse events. Adverse events in patients who received a tyrosine kinase inhibitor (TKI) post-ICI were also captured.
UNASSIGNED: A total of 246 patients were identified, 170 treated with C plus ICI and 76 treated with C alone. Driver alterations included EGFR (54.9%), KRAS (32.9%), ALK (5.3%), HER2/ERBB2 (2.9%), ROS1 (1.2%), MET (1.2%), RET (0.8%), and BRAF non-V600 (0.8%). The overall PFS and OS hazard ratios were not significant at 1.12 (95% confidence interval 0.83-1.51; p = 0.472) and 0.86 (95% confidence interval: 0.60-1.24, p = 0.429), respectively. No significant differences in PFS or OS were observed in the mutational subgroups. Grade 3 or greater adverse events were lower in the C plus ICI group. The multivariate analysis for PFS and OS revealed a performance status (Eastern Cooperative Oncology Group) score of 2, and previous TKI treatment was associated with poorer outcomes with C plus ICI.
UNASSIGNED: Our study suggests that patients with oncogenic-driven NSCLC, primarily those with EGFR-driven tumors, treated with a TKI should not subsequently receive C plus ICI. Analysis from prospective clinical trials will provide additional information on the role of ICIs in this group of patients.
摘要：
UNASSIGNED：关于免疫检查点抑制剂（ICIs）加双重化疗（C）治疗晚期肺癌患者的数据很少，其肿瘤具有可操作的突变。我们试图深入了解该组合在该患者人群中与单独化疗有关的作用。
UNASSIGNED：我们在加州大学国家癌症研究所的五个指定的综合癌症中心进行了一项回顾性研究。主要终点是无进展生存期（PFS）。次要终点包括总生存期(OS)和显著不良事件。还捕获了ICI后接受酪氨酸激酶抑制剂（TKI）的患者的不良事件。
未经批准：共确定了246名患者，用C加ICI处理的170和用单独的C处理的76。驱动改变包括EGFR（54.9%），KRAS（32.9%），ALK（5.3%），HER2/ERBB2（2.9%），ROS1（1.2%），MET（1.2%），RET（0.8%），和BRAF非V600（0.8%）。总体PFS和OS风险比在1.12（95％置信区间0.83-1.51；p=0.472）和0.86（95％置信区间：0.60-1.24，p=0.429）不显著，分别。在突变亚组中没有观察到PFS或OS的显着差异。C加ICI组的3级或更高的不良事件较低。PFS和OS的多变量分析显示，表现状态（东部肿瘤协作组）得分为2，以前的TKI治疗与C加ICI的较差预后相关。
未经证实：我们的研究表明，致癌驱动的非小细胞肺癌患者，主要是那些EGFR驱动的肿瘤，用TKI治疗后不应该接受C加ICI。前瞻性临床试验的分析将提供有关ICI在该组患者中的作用的其他信息。
UNASSIGNED：我们在加州大学国家癌症研究所的五个指定的综合癌症中心进行了一项回顾性研究。主要终点是无进展生存期（PFS）。次要终点包括总生存期(OS)和显著不良事件。还捕获了ICI后接受酪氨酸激酶抑制剂（TKI）的患者的不良事件。
未经批准：共确定了246名患者，用C加ICI处理的170和用单独的C处理的76。驱动改变包括EGFR（54.9%），KRAS（32.9%），ALK（5.3%），HER2/ERBB2（2.9%），ROS1（1.2%），MET（1.2%），RET（0.8%），和BRAF非V600（0.8%）。总体PFS和OS风险比在1.12（95％置信区间0.83-1.51；p=0.472）和0.86（95％置信区间：0.60-1.24，p=0.429）不显著，分别。在突变亚组中没有观察到PFS或OS的显着差异。C加ICI组的3级或更高的不良事件较低。PFS和OS的多变量分析显示，表现状态（东部肿瘤协作组）得分为2，以前的TKI治疗与C加ICI的较差预后相关。
未经证实：我们的研究表明，致癌驱动的非小细胞肺癌患者，主要是那些EGFR驱动的肿瘤，用TKI治疗后不应该接受C加ICI。前瞻性临床试验的分析将提供有关ICI在该组患者中的作用的其他信息。
