LAUSR

To predict epidermal growth factor receptor (EGFR) mutation status in lung adenocarcinoma using MR-based radiomics signature of brain metastasis and explore the optimal MR sequence for prediction. Data from 52 patients with brain metastasis from lung adenocarcinoma (28 with mutant EGFR, 24 with wild-type EGFR) were retrospectively reviewed. Contrast-enhanced T1-weighted imaging (T1-CE), T2 fluid-attenuated inversion recovery (T2-FLAIR), T2WI, and DWI sequences were selected for radiomics features extraction. A total of 438 radiomics features were extracted from each MR sequence. All sequences were randomly divided into training and validation cohorts. The least absolute shrinkage selection operator was used to select informative features, a radiomics signature was built with the logistic regression model of the training cohort, and the radiomics signature performance was evaluated using the validation cohort and an independent testing data set. The radiomics signature built on 9 selected features showed good discrimination in both the training and validation cohorts for T2-FLAIR. The radiomics signature of T2-FLAIR yielded an AUC of 0.987, a classification accuracy of 0.991, sensitivity of 1.000, and specificity of 0.980 in the validation cohort. The AUC was 0.871 in the independent testing data set. The AUCs of our radiomics signature to differentiate exon 19 and exon 21 mutations were 0.529, 0.580, 0.645, and 0.406 for T1-CE, T2-FLAIR, T2WI, and DWI, respectively. We developed a T2-FLAIR radiomics signature that can be used as a noninvasive auxiliary tool for predicting EGFR mutation status in lung adenocarcinoma, which is helpful to guide therapeutic strategies. • MR-based radiomics signature of brain metastasis may help predict EGFR mutation status in lung adenocarcinoma, especially using T2-FLAIR. • Nine radiomics features extracted from T2-FLAIR sequence strongly correlate with EGFR mutation status. • Radiomics features reflect tumor heterogeneity through potential changes in tissue morphology caused by EGFR mutation.