Advanced Lung Adenocarcinoma Harboring a Mutation of the Epidermal Growth Factor Receptor: CT Findings after Tyrosine Kinase Inhibitor Therapy

被引:37
作者
Choi, Chang-Min [1 ,2 ]
Kim, Mi Young [3 ,4 ]
Lee, Jae Cheol [2 ]
Kim, Hwa Jung [5 ]
机构
[1] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pulm & Crit Care Med, Seoul 138736, South Korea
[2] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Oncol, Seoul 138736, South Korea
[3] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Radiol, Seoul 138736, South Korea
[4] Univ Ulsan, Coll Med, Asan Med Ctr, Res Inst Radiol, Seoul 138736, South Korea
[5] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Clin Epidemiol & Biostat, Seoul 138736, South Korea
关键词
CANCER; GEFITINIB; ERLOTINIB;
D O I
10.1148/radiol.13121824
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Purpose: To study chest computed tomography (CT) in tyrosine kinase inhibitor (TKI) treatment of epidermal growth factor receptor (EGFR)-mutant adenocarcinoma. Materials and Methods: 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. Results: 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). Conclusion: Smaller nodular lesions, peripheral lesions, and 19del relate to longer PFS after EGFR TKI treatment. (C) RSNA, 2013
引用
收藏
页码:574 / 582
页数:9
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