评估EGFR突变晚期非小细胞肺癌接受TKIs治疗的患者中TP53突变的预后影响。选择研究探讨接受TKIs治疗的EGFR突变/TP53野生型患者与EGFR/TP53共突变患者的临床结果。采用固定和随机效应模型积累数据。总共有29项试验符合条件。PFS分析显示，TP53共突变组的PFS较EGFR突变/TP53野生型组更短(HR = 1.67，95% CI 1.51-1.83，异质性I2 =20%，p = 0.18)。EGFR/TP53共突变NSCLC患者有更高的死亡风险（HR=1.89，95% CI 1.67-2.14，异质性I2 =21％，p = 0.19）。子组分析显示，第一和第二代TKIs以及第三代TKIs在PFS和OS方面的差异并不显著（p = 0.31，p = 0.08）。TP53突变代表EGFR-TKIs抵抗的一个临床相关机制，无论是哪一代。应该在专门的临床试验中探索个性化治疗方法。 版权所有©2023 Elsevier B.V.。

To assess the prognostic impact of TP53 mutations in EGFR-mutant advanced NSCLC patients treated with TKIs.Studies exploring the clinical outcomes of EGFR mutant/TP53 wild-type versus EGFR/TP53 co-mutant patients treated with TKIs were selected. Data were cumulated by adopting a fixed and random-effect model.Overall, 29 trials were eligible. The PFS analysis showed that TP53 co-mutant group has shorter PFS versus EGFR mutant/TP53 wild-type group (HR = 1.67, 95% CI 1.51-1.83, heterogeneity I2 =20%, p = 0.18). Patients affected by EGFR/TP53 co-mutant NSCLC have a higher chance of shorter OS versus EGFR mutant/TP53 wild type (HR= 1.89, 95% CI 1.67-2.14, heterogeneity I2 = 21%; p = 0.19). The subgroup analysis showed no significant difference between first-second versus third-generation TKIs in both PFS and OS (p = 0.31, p = 0.08).TP53 mutations represent a clinically relevant mechanism of resistance to EGFR-TKIs, regardless of their generation. A personalized therapeutical approach should be explored in dedicated clinical trials.Copyright © 2023 Elsevier B.V. All rights reserved.