目的:HER2是非小细胞肺癌(NSCLC)中罕见突变的驱动基因。目前,尚无全面的大规模临床研究来确定HER2突变体晚期肺腺癌(LUAD)的最佳一线治疗策略.除此之外,吡唑替尼的有效性和安全性,泛HER抑制剂,在NSCLC的背景下仍在研究中。
方法:在本研究中,我们对2014年5月至2023年6月期间接受一线治疗和吡罗替尼治疗的HER2突变晚期LUAD进行了回顾性数据收集.接受化疗的患者,化疗+免疫检查点抑制剂(ICIs),化疗+贝伐单抗和吡罗替尼的一线治疗.此外,我们收集了这些患者疾病进展后使用吡唑替尼的疗效和安全性数据.研究的主要终点是无进展生存期(PFS)。
结果:在最终分析中,89例患者纳入一线队列,30例患者纳入吡唑替尼队列。在一线治疗队列中,化疗+ICIs,化疗+贝伐单抗,与化疗相比,吡唑替尼表现出显著的生存获益(中位PFS:9.87vs.7.77vs.7.10vs.5.40个月,p值<0.05)。此外,一线治疗PFS少于6个月的患者可能会从随后的pyrotinib治疗中受益(中位PFS:7.467vs.3.000,p值=0.0490)。
结论:在HER2突变体LUAD的一线治疗中,涉及化疗+ICIs等组合的方案,化疗+贝伐单抗,与化疗相比,吡唑替尼可能具有增强的生存优势。然而,在这三种治疗策略中没有观察到明显的区别,强调必须识别生物标志物,以辨别选择合适的治疗方式。此外,一线治疗疗效欠佳的患者可能会从吡罗替尼获得更多益处.
OBJECTIVE: HER2 is an infrequently mutated driver gene in non-small cell lung cancer (NSCLC). At present, there has been no comprehensive large-scale clinical study to establish the optimal first-line treatment strategy for advanced lung adenocarcinoma (LUAD) with HER2-Mutant. Besides that, the effectiveness and safety of pyrotinib, a pan-HER inhibitor, in the context of NSCLC are still undergoing investigation.
METHODS: In this study, we conducted a retrospective data collection of HER2-Mutated advanced LUAD who received first-line treatment and pyrotinib between May 2014 and June 2023. Patients treated with chemotherapy, chemotherapy + immune checkpoint inhibitors (ICIs), chemotherapy +
bevacizumab and pyrotinib in first-line treatment. Furthermore, we collected data on the efficacy and safety of pyrotinib in these patients after disease progression. The main endpoint of the study was progression-free survival (PFS).
RESULTS: In the final analysis, 89 patients were included in the first-line cohort and 30 patients were included in the pyrotinib cohort. In the first-line treatment cohort, chemotherapy + ICIs, chemotherapy +
bevacizumab, and pyrotinib exhibited notable survival benefits compared to chemotherapy (median PFS: 9.87 vs. 7.77 vs. 7.10 vs. 5.40 months, p-value < 0.05). Furthermore, patients with a first-line treatment PFS of less than 6 months may potentially benefit from subsequent treatment with pyrotinib (median PFS: 7.467 vs. 3.000, p-value = 0.0490).
CONCLUSIONS: In the first-line treatment of HER2-Mutant LUAD, regimens involving combinations like chemotherapy + ICIs, chemotherapy +
bevacizumab, and pyrotinib may confer enhanced survival advantages compared to chemotherapy. Nevertheless, no significant distinctions were observed among these three treatment strategies, underscoring the imperative to identify biomarkers for the discerning selection of suitable therapeutic modalities. Moreover, patients with suboptimal response to first-line treatment may potentially derive more benefit from pyrotinib.