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Q. Cai



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    P2.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 234)

    • Event: WCLC 2015
    • Type: Poster
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      P2.04-010 - 18F-FDG Uptake and CEA between Different EGFR Mutations in Patients with Non-Small Cell Lung Cancer (ID 1413)

      09:30 - 09:30  |  Author(s): Q. Cai

      • Abstract
      • Slides

      Background:
      Many studies have demonstrated the clinical efficacy of the epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) gefitinib and erlotinib compared with chemotherapy against non–small-cell lung cancer (NSCLC) when used as first-line treatment for patients whose tumors harbor activating EGFR mutations. But sometimes the acquisition of adequate tissues for EGFR mutation analysis is not feasible. The aim of this study is to evaluate the relationship between EGFR mutation status, serum carcinoembryonic antigen (CEA) levels, and the SUVmax of [[18]F]-fluorodeoxyglucose positron emission tomography (FDG-PET) in primary disease and metastatic lymph nodes, and in Chinese non-small cell lung cancer patients.

      Methods:
      From January 2009 and October 2010, 167 patients with definite pathological diagnosis of NSCLC who underwent [[18]F]-FDG-PET, EGFR mutation analysis by amplification refractory mutation system (ARMOS) method, and CEA value by Elecsys chemiluminescence immunoassay system were eligible to participate in this study. The associations of EGFR mutation status with patient characteristics, maximal standard uptake value (SUVmax) of primary tumors and metastatic lymph nodes, serum CEA level at diagnosis were analyzed. Receiver-operating characteristic (ROC) curve analysis was performed to quantify the predictive value of these factors. Multivariate logistic regression analysis was used to analyze predictors of EGFR mutations.

      Results:
      EGFR mutations were identified in 167 patients (73 EGFR-mutant and 94 wild-type). The [[18]F]-FDG uptake was significantly lower in EGFR-mutant (mean SUVmax=9.3) than wild-type (10.2) NSCLC patients (P=0.045). The CEA value was significantly higher in EGFR-mutant (mean CEA=12.5) than wild-type (5.8) NSCLC patients (P=0.030). The ROC analysis concluded that high FDG uptake (SUV≥9.6) may be predictive of the wild-type EGFR genotype, whereas a low normalized SUVmax may predict the presence of EGFR mutations less robustly. We also demonstrated that high CEA levels (CEA≥9.25) were positively correlated with histological EGFR gene mutations by ROC analysis. On multivariate analysis, non-smoker, the low SUVmax of the primary tumor and the high CEA value were significantly associated with EGFR mutation status. In addition, we also showed that the exon 19 mutation (mean SUVmax=10.6) is strongly correlated with higher SUVmax than exon 21 mutation (mean SUVmax=8.7) (P=0.017). The metastatic lymph nodes in EGFR-mutant patients had lower SUVmax than EGFR wild-type patients (SUVmax 7.3 vs 6.65, P < 0.001).

      Conclusion:
      The combined evaluation of SUVmax FDG uptake in primary tumor and metastatic lymph nodes, CEA level, and smoking status may be helpful in predicting EGFR mutation status in patients with NSCLC, especially when the tumor sample is inadequate for genetic analysis or genetic testing is not available.

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