Monitoring of carcinoembryonic antigen levels is predictive of EGFR mutations and efficacy of EGFR-TKI in patients with lung adenocarcinoma
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  • 作者:Yanwei Zhang (1)
    Bo Jin (1)
    Minhua Shao (1)
    Yu Dong (1)
    Yuqing Lou (1)
    Aimi Huang (1)
    Baohui Han (1)
  • 关键词:Lung adenocarcinoma ; Carcinoembryonic antigen ; EGFR mutations ; ARMS
  • 刊名:Tumor Biology
  • 出版年:2014
  • 出版时间:May 2014
  • 年:2014
  • 卷:35
  • 期:5
  • 页码:4921-4928
  • 全文大小:
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  • 作者单位:Yanwei Zhang (1)
    Bo Jin (1)
    Minhua Shao (1)
    Yu Dong (1)
    Yuqing Lou (1)
    Aimi Huang (1)
    Baohui Han (1)

    1. Department of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 West Huai Hai Road, Shanghai, People’s Republic of China
  • ISSN:1423-0380
文摘
For the detection of epidermal growth factor receptor (EGFR) mutations, tumor tissues may not always be available. Not all the patients harboring EGFR mutation have a clinical response after the treatment of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI). EGFR mutations were detected in 70 cases of newly diagnosed non-smoking adenocarcinoma, and patients harboring EGFR mutations received EGFR-TKI treatment. The EGFR mutation status of these patients-blood was analyzed by amplification refractory mutation system (ARMS). The patients-carcinoembryonic antigen (CEA) levels were tested on the third, seventh, 15th, and 30th days after EGFR-TKI treatment. Forty-four cases were found with EGFR mutations. EGFR mutation rate of CEA high-level group was significantly higher than low-level group (70.8?% vs. 40.9?%, P--.017). Multivariate analysis showed that high-level CEA is independently associated with EGFR gene mutation (P--.020, OR--.508, 95?%CI, 1.223-0.059). The sensitivity of high CEA level and ARMS to predict EGFR mutation were 79.1?% and 51.2?%. We divided the patients who received EGFR-TKI treatment into three groups by the variation types of CEA. Univariate analysis showed that patients in descending type group have longer progression-free survival (P--.001, HR 6.981, 95?%CI, 2.534-9.237). Multivariate Cox proportional hazards model analyses shows the same result (P--.001, HR 9.82, 95?%CI, 3.322-26.031). In conditions of the current technique, using high CEA level to predict EGFR mutations seems to be more sensitive than using EGFR mutations in plasma. The variation types of CEA level could help us to predict the efficacy of EGFR-TKI in patients harboring EGFR mutation within only 1?month of tyrosine kinase inhibitor therapy.
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