Division of Pulmonary and Critical Care, Department of Internal Medicine, China Medical University Hospital, No. 2, Yude Road, North District, Taichung City, 40402, Taiwan.
Division of Hematology and Oncology, Department of Internal Medicine, China Medical University Hospital, No. 2, Yude Road, North District, Taichung City, 40402, Taiwan.
BMC Cancer. 2022 May 23;22(1):571. doi: 10.1186/s12885-022-09672-4.
The addition of anti-angiogenesis drugs to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) or chemotherapy in patients with EGFR-mutant non-small cell lung cancer (NSCLC) can improve disease control. We conducted a study to evaluate the efficacy of combination therapeutic strategies and identify patients who could benefit from combination therapy.
This study enrolled patients with stage IV EGFR-mutant NSCLC treated with first-line EGFR-TKIs between January 2014 and December 2020. We divided patients into three groups: patients who received an anti-angiogenesis drug as first-line combination therapy, those who received an anti-angiogenesis drug as further-line combination therapy, and those with no anti-angiogenesis therapy.
A total of 204 patients were enrolled in the final analysis. Progression-free survival (PFS) in patients receiving first-line anti-angiogenesis plus EGFR-TKI combination therapy was longer (18.2 months) than those treated with first-line EGFR-TKI monotherapy (10.0 months for both, p < 0.001). No difference in overall survival (OS) was observed among these three groups (30.5 vs. 42.6 vs. 33.7 months, p = 0.326). Multivariate Cox regression analysis revealed L858R mutation, pleural, liver, and bone metastasis as independent prognostic factors for poor OS. However, the addition of anti-angiogenesis therapy to patients with these poor prognostic factors improved OS to levels similar to those without these poor prognostic factors.
First-line combination EGFR-TKI plus anti-angiogenesis therapy improves PFS in patients with stage IV EGFR-mutant NSCLC. Adding an anti-angiogenesis drug at any line to patients harboring L858R mutation with pleural, liver, or bone metastases can provide survival benefits.
在表皮生长因子受体（EGFR）-酪氨酸激酶抑制剂（TKI）或化疗中加入抗血管生成药物可改善 EGFR 突变型非小细胞肺癌（NSCLC）患者的疾病控制。我们进行了一项研究，以评估联合治疗策略的疗效，并确定哪些患者可以从联合治疗中受益。
本研究纳入了 2014 年 1 月至 2020 年 12 月期间接受一线 EGFR-TKI 治疗的 IV 期 EGFR 突变型 NSCLC 患者。我们将患者分为三组：一线联合治疗中接受抗血管生成药物治疗的患者、二线联合治疗中接受抗血管生成药物治疗的患者和未接受抗血管生成治疗的患者。
共有 204 例患者最终纳入分析。一线抗血管生成联合 EGFR-TKI 治疗组的无进展生存期（PFS）较长（18.2 个月），而一线 EGFR-TKI 单药治疗组的 PFS 较短（10.0 个月，均为 p<0.001）。三组之间的总生存期（OS）无差异（30.5 个月比 42.6 个月比 33.7 个月，p=0.326）。多变量 Cox 回归分析显示 L858R 突变、胸膜、肝脏和骨转移是 OS 不良的独立预后因素。然而，将抗血管生成治疗加入到具有这些不良预后因素的患者中，可将 OS 改善至与无这些不良预后因素的患者相似的水平。
一线联合 EGFR-TKI 加抗血管生成治疗可改善 IV 期 EGFR 突变型 NSCLC 患者的 PFS。将抗血管生成药物添加到具有胸膜、肝脏或骨转移的 L858R 突变患者的任何一线治疗中都可以提供生存获益。
