Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Clinical Development and Medical Affairs, Roche Diagnostic Solutions, Pleasanton, California, United States of America.
PLoS One. 2022 Apr 28;17(4):e0267362. doi: 10.1371/journal.pone.0267362. eCollection 2022.
15-40% of non-small cell lung cancer (NSCLC) patients harbor epidermal growth factor receptor (EGFR)-sensitizing mutations. Tyrosine kinase inhibitors (TKIs) provide significant clinical benefit in this population, yet all patients will ultimately progress. Liquid biopsy can reliably identify somatic tumor-associated EGFR mutations in plasma. This study aimed to assess the feasibility and value of the quantitative assessment of EGFR driver mutations in plasma in EGFR-mutated NSCLC patients treated with EGFR-TKIs as a tool to evaluate therapeutic response to TKIs and monitor for disease progression. The study included 136 patients with tissue biopsy-confirmed EGFR-sensitizing, mutation-positive lung adenocarcinoma with plasma collected prior to TKI treatment and at least two post-initiation TKI treatment/follow-up blood samples. Plasma samples were tested with the cobas® EGFR Mutation Test v2 (cobas EGFR Test), and semi-quantitative index (SQI) values for each identified mutation were reported by the assay software. The most common baseline EGFR mutations detected in tissue were L858R (53.7%) and exon 19 deletion (39.7%). Plasma cell-free DNA analysis detected EGFR mutations in 74% of the baseline samples. Objective response rate by RECIST 1.1 was achieved in 72% of patients, while 93% had a molecular response (defined as disappearance of the EGFR mutation from plasma). 83% of patients had molecular progression (MP; 1.5X SQI increase or new T790M mutation), and 82% who had a clinical response had clinical progression. On average, MP occurred 42 days prior to clinical progression. Patients who progressed while on first-line TKI showed MP of the original EGFR-sensitizing mutations prior to the emergence of a T790M mutation, which was detected in 27% of the EGFR plasma-positive patients. Longitudinal monitoring of EGFR mutational load in plasma is feasible and can predict both response and clinical progression in EGFR-mutated NSCLC patients treated with EGFR-TKIs, as well as detect treatment-emergent EGFR mutations.
15-40%的非小细胞肺癌(NSCLC)患者携带表皮生长因子受体(EGFR)敏化突变。在这部分人群中,酪氨酸激酶抑制剂(TKI)可提供显著的临床获益,但所有患者最终都会进展。液体活检可可靠地在血浆中鉴定出与肿瘤相关的 EGFR 体细胞突变。本研究旨在评估定量评估 EGFR 驱动突变在 EGFR-TKI 治疗的 EGFR 突变型 NSCLC 患者中的血浆作为评估 TKI 治疗反应和监测疾病进展的工具的可行性和价值。该研究纳入了 136 例经组织活检证实为 EGFR 敏化、突变阳性的肺腺癌患者,这些患者在 TKI 治疗前和至少两次 TKI 治疗/随访时采集了血浆样本。采用 cobas® EGFR Mutation Test v2(cobas EGFR Test)对血浆样本进行检测,检测软件报告了每个鉴定出的突变的半定量指数(SQI)值。组织中最常见的基线 EGFR 突变是 L858R(53.7%)和外显子 19 缺失(39.7%)。血浆无细胞 DNA 分析检测到 74%的基线样本中存在 EGFR 突变。根据 RECIST 1.1 标准,客观缓解率为 72%,而 93%的患者有分子缓解(定义为血浆中 EGFR 突变消失)。83%的患者有分子进展(MP;SQI 增加 1.5 倍或出现新的 T790M 突变),82%有临床反应的患者有临床进展。平均而言,MP 发生在临床进展前 42 天。在一线 TKI 治疗期间进展的患者在出现 T790M 突变之前出现了原始 EGFR 敏化突变的 MP,在 27%的 EGFR 血浆阳性患者中检测到了该突变。对 EGFR 突变负荷的纵向监测在 EGFR-TKI 治疗的 EGFR 突变型 NSCLC 患者中是可行的,可预测反应和临床进展,并可检测治疗出现的 EGFR 突变。