Correlation of 18F-FDG uptake and EGFR/KRAS mutations in surgically resected lung cancer.

Abstract

10547 Background: The mutation status of both the epidermal growth factor receptor (EGFR) and KRAS genes have been reported to be important predictors of the efficacy of EGFR tyrosine kinase inhibitors such as gefitinib or erlotinib. 18F-fluoro-2-deoxy-glucose (18F-FDG) positron emission tomography (PET) is a functional imaging modality based on glucose metabolism, which has recently been used as a common staging tool for non-small cell lung cancer. We investigated the correlations between the standardized uptake value (SUV) of 18F-FDG and the mutation status of the EGFR and KRAS genes in lung cancer. Methods: We conducted a retrospective review of 189 patients with surgically resected lung cancers (167 adenocarcinomas and 22 non-adenocarcinomas) who underwent 18F-FDG PET/computed tomography scans preoperatively and who were examined for EGFR/KRAS mutations using surgically resected specimens. Correlations between the EGFR/KRAS mutation status and the clinicopathological factors including SUVmax were examined by the chi-square test and a logistic regression analysis. Results: EGFR and K-ras mutations were detected in 82 (44%) and 21 (11%) of the 189 lung cancers, respectively. The univariate analyses showed that EGFR mutations were more frequently observed in females (61%), non-smokers (56%), adenocarcinomas (49%), tumors ≤3 cm (51%), tumors without lymph node involvement (49%), lymphatic permeation (53%) and blood vessel invasion (53%), and with SUVmax <10 (51%). In the multivariate analyses, gender and SUVmax were the significant predictors of EGFR mutation. In the 75 female patients with a tumor with SUVmax <10, 49 (65%) patients had EGFR mutations. The univariate analyses showed that KRAS mutations were more frequently observed in males (17%), smokers (16%), and tumors with SUVmax ≥10 (21%). In the multivariate analyses, only gender was a significant predictor of KRAS mutations. Conclusions: The probability of EGFR mutation was inversely correlated with the SUVmax. In contrast, the probability of KRAS mutation was directly correlated with the SUVmax. EGFR mutated lung cancer may therefore be biologically less aggressive than KRAS mutated lung cancer.