From the Department of Pulmonary and Critical Care Medicine (C.M.C.), Department of Oncology (C.M.C., J.C.L.), Department of Radiology and Research Institute of Radiology (M.Y.K.), and Department of Clinical Epidemiology and Biostatistics (H.J.K.), University of Ulsan College of Medicine, Asan Medical Center, 86 Asanbyeongwon-Gil, Songpa-Gu, Seoul 138-736, Korea.
Radiology. 2014 Feb;270(2):574-82. doi: 10.1148/radiol.13121824. Epub 2013 Oct 28.
To study chest computed tomography (CT) in tyrosine kinase inhibitor (TKI) treatment of epidermal growth factor receptor (EGFR)-mutant adenocarcinoma.
This retrospective study was approved by the institutional review board. Informed consent was waived. One hundred thirty consecutive patients with stage IV adenocarcinoma and EGFR mutations at a single tertiary center from November 2004 to April 2010 were enrolled retrospectively. CT images were analyzed with Response Evaluation Criteria in Solid Tumor guidelines. Target lesions were classified by size, type, axial location, and metastasis. Patients were followed after TKI therapy, and treatment response was classified as partial response, stable disease, or progressive disease. A Cox proportional hazards model was used to correlate baseline CT features and EGFR mutations with progression-free survival (PFS) and overall survival.
All patients underwent TKI therapy after identifying exon mutations in the EGFR gene, comprising exon 19 deletion (19del) (n = 77), L858R (n = 43), and exon 18 (n = 10). Outcomes were partial response (n = 103), stable disease (n = 22), and progressive disease (n = 5). In univariate analysis, PFS was significantly longer with small lesions (hazard ratio [HR], 1.02; 95% confidence interval [CI]: 1.01, 1.03; P < .01), nodular main lesions (HR, 0.55; 95% CI: 0.34, 0.88; P = .01), or peripheral lesions (HR, 0.62; 95% CI: 0.42, 0.93; P = .02). In univariate analysis, PFS was significantly longer with smaller lesions (HR, 1.02; 95% CI: 1.01, 1.03; P < .01), nodular main lesions (HR, 0.55; 95% CI: 0.34, 0.88; P = .01), peripheral lesions (HR, 0.62; 95% CI: 0.42, 0.93; P = .02), 19del (HR, 0.33; 95% CI: 0.14, 0.77; P = .01), or L858R (HR, 0.39; 95% CI: 0.16, 0.97; P = .04). In multivariate analysis, PFS was significantly longer with 19del (HR, 0.30; 95% CI: 0.11, 0.84; P = .02) and shorter with scattered metastases (HR, 2.25; 95% CI: 1.44, 5.51; P < .01).
Smaller nodular lesions, peripheral lesions, and 19del relate to longer PFS after EGFR TKI treatment.
研究表皮生长因子受体（EGFR）突变型腺癌患者接受酪氨酸激酶抑制剂（TKI）治疗时的胸部计算机断层扫描（CT）。
本回顾性研究经机构审查委员会批准。豁免了知情同意。2004 年 11 月至 2010 年 4 月，从一家三级医疗中心招募了 130 名患有 IV 期腺癌且 EGFR 突变的连续患者。使用实体瘤反应评估标准分析 CT 图像。根据大小、类型、轴向位置和转移对靶病变进行分类。在 TKI 治疗后对患者进行随访，并将治疗反应分类为部分缓解、稳定疾病或进展性疾病。使用 Cox 比例风险模型将基线 CT 特征和 EGFR 突变与无进展生存期（PFS）和总生存期相关联。
所有患者在鉴定出 EGFR 基因外显子突变后均接受了 TKI 治疗，包括外显子 19 缺失（19del）（n = 77）、L858R（n = 43）和外显子 18（n = 10）。结果为部分缓解（n = 103）、稳定疾病（n = 22）和进展性疾病（n = 5）。在单变量分析中，PFS 与小病变（风险比 [HR]，1.02；95%置信区间 [CI]：1.01，1.03；P <.01）、结节状主病变（HR，0.55；95%CI：0.34，0.88；P =.01）或周围病变（HR，0.62；95%CI：0.42，0.93；P =.02）显著相关。在单变量分析中，PFS 与较小病变（HR，1.02；95%CI：1.01，1.03；P <.01）、结节状主病变（HR，0.55；95%CI：0.34，0.88；P =.01）、周围病变（HR，0.62；95%CI：0.42，0.93；P =.02）、19del（HR，0.33；95%CI：0.14，0.77；P =.01）或 L858R（HR，0.39；95%CI：0.16，0.97；P =.04）显著相关。在多变量分析中，19del 与较长的 PFS 显著相关（HR，0.30；95%CI：0.11，0.84；P =.02），而散发性转移与较短的 PFS 显著相关（HR，2.25；95%CI：1.44，5.51；P <.01）。
较小的结节状病变、周围病变和 19del 与 EGFR TKI 治疗后较长的 PFS 相关。
