Open AccessThe detection of EGFR mutation status in plasma is reproducible and can dynamically predict the efficacy of EGFR‐TKI
Author(s) -
Huang Zhen,
Wang Zhijie,
Bai Hua,
Wu Meina,
An Tongtong,
Zhao Jun,
Yang Lu,
Duan Jianchun,
Zhuo Minglei,
Wang Yuyan,
Wang Shuhang,
Wang Jie
Publication year - 2012
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/j.1759-7714.2012.00133.x
Subject(s) - concordance , medicine , epidermal growth factor receptor , mutation , oncology , lung cancer , epidermal growth factor , targeted therapy , tyrosine kinase inhibitor , cancer research , cancer , receptor , gene , biology , genetics
Background: The validity of epidermal growth factor receptor (EGFR) mutation in serum and plasma DNA as a surrogate of tumor tissue has been comprehensively explored. However, the concordance between peripheral blood and tumor tissue samples in EGFR mutation detection remains variable. The question as to whether real‐time samples for EGFR mutation analysis are required before epidermal growth factor receptor tyrosine kinase inhibitor (EGFR‐TKI) therapy remains unanswered. Methods: This study included two cohorts:(i) 822 non‐small cell lung cancer (NSCLC) patients with primary tumor tissue and matched plasma samples at initial diagnosis; and (ii) 207 patients with advanced NSCLC who had plasma samples taken immediately before EGFR‐TKI therapy, in which 157 cases had matched tumor tissues. Denaturing High‐Performance Liquid Chromatography (DHPLC) determined EGFR mutation status. Results: Among a total of 822 patients with matched samples, the EGFR mutation rates were 36.3% and 32.1% in tissue and plasma samples, respectively. Concordance of EGFR mutation between two kinds of samples was 77.0% (631/822),with 63.5% (188/296) of accuracy of EGFR mutation in plasma DNA. In 207 advanced NSCLC patients who had plasma samples taken immediately before EGFR‐TKI therapy, the objective response rate (ORR) after EGFR‐TKI therapy was significantly higher in EGFR mutant patients than those in EGFR wild‐type patients (51.4% vs. 22.6%, P < 0.001), regardless of the treatment lines of EGFR‐TKI. In patients with two or more lines of EGFR‐TKI therapy, EGFR mutation status in plasma samples, but not in tissues, was a predictor for progression‐free survival (PFS) after EGFR‐TKI therapy (mutant vs. wild‐type: 10.1 months vs. 3.7 months, P = 0.038). Conclusions: An EGFR mutation test using plasma DNA samples was validated and reproducible. Obtaining real‐time samples for EGFR mutation detection is critical in order to predict the outcomes of EGFR‐TKI.