Abstract
Purpose
We aim to compare the radiomic features and parameters on 2-deoxy-2-[fluorine-18] fluoro-D-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) between patients with endometrial cancer with Lynch syndrome and those with endometrial cancer without Lynch syndrome. We also hope to explore the biologic significance of selected radiomic features.
Materials and Methods
We conducted a retrospective cohort study, first using the 18F-FDG PET/CT images and clinical data from 100 patients with endometrial cancer to construct a training group (70 patients) and a test group (30 patients). The metabolic parameters and radiomic features of each tumor were compared between patients with and without Lynch syndrome. An independent cohort of 23 patients with solid tumors was used to evaluate the value of selected radiomic features in predicting the expression of the programmed cell death 1 (PD1), using 18F-FDG PET/CT images and RNA-seq genomic data.
Results
There was no statistically significant difference in the standardized uptake values on PET between patients with endometrial cancer with Lynch syndrome and those with endometrial cancer without Lynch syndrome. However, there were significant differences between the 2 groups in metabolic tumor volume and total lesion glycolysis (p < 0.005). There was a difference in the radiomic feature of gray level co-occurrence matrix entropy (GLCMEntropy; p < 0.001) between the groups: the area under the curve was 0.94 in the training group (sensitivity, 82.86%; specificity, 97.14%) and 0.893 in the test group (sensitivity, 80%; specificity, 93.33%). In the independent cohort of 23 patients, differences in GLCMEntropy were related to the expression of PD1 (r(s) =0.577; p < 0.001).
Conclusions
In patients with endometrial cancer, higher metabolic tumor volumes, total lesion glycolysis values, and GLCMEntropy values on 18F-FDG PET/CT could suggest a higher risk for Lynch syndrome. The radiomic feature of GLCMEntropy for tumors is a potential predictor of PD1 expression.