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Objectives To develop a radiomics signature for predicting surgical portal vein-superior mesenteric vein (PV-SMV) in patients with pancreatic ductal adenocarcinoma (PDAC) and measure the effect of providing the predictions of radiomics signature to radiologists with different diagnostic experiences during imaging interpretation. Methods Between February 2008 and June 2020, 146 patients with PDAC in pancreatic head or uncinate process from two institutions were retrospectively included and randomly split into a training (n = 88) and a validation (n =58) cohort. Intraoperative vascular exploration findings were used to identify surgical PV-SMV invasion. Radiomics features were extracted from the portal venous phase CT images. Radiomics signature was built with a linear elastic-net regression model. Area under receiver operating characteristic curve (AUC) of the radiomics signature was calculated. A senior and a junior radiologist independently review CT scans and made the diagnosis for PV-SMV invasion both with and without radiomics score (Radscore) assistance. A 2-sided Pearson's chi-squared test was conducted to evaluate whether there was a difference in sensitivity, specificity, and accuracy between the radiomics signature and the unassisted radiologists. To assess the incremental value of providing Radscore predictions to the radiologists, we compared the performance between unassisted evaluation and Radscore-assisted evaluation by using the McNemar test. Results Numbers of patients identified as presence of surgical PV-SMV invasion were 33 (37.5%) and 19 (32.8%) in the training and validation cohort, respectively. The radiomics signature achieved an AUC of 0.848 (95% confidence interval, 0.724-0.971) in the validation cohort and had a comparable sensitivity, specificity, and accuracy as the senior radiologist in predicting PV-SMV invasion (all p-values > 0.05). Providing predictions of radiomics signature increased both radiologists' sensitivity in identifying PV-SMV invasion, while only the increase of the junior radiologist was significant (63.2 vs 89.5%, p-value = 0.025) instead of the senior radiologist (73.7 vs 89.5%, p-value = 0.08). Both radiologists' accuracy had no significant increase when provided radiomics signature assistance (both p-values > 0.05). Conclusions The radiomics signature can predict surgical PV-SMV invasion in patients with PDAC and may have incremental value to the diagnostic performance of radiologists during imaging interpretation.

Gastric cancer (GC) remains one of the most lethal human malignancies, and exploring novel therapeutic targets for the treatment has been a major focus. The molecular mechanism of invasion and migration of GC cells remains unclear. The present study aimed to investigate the role of Tensin 4 and the associated molecular signaling pathways in the process of invasion and metastasis of GC. The expression of Tensin 4 protein and phosphorylated AKT (p-AKT) were evaluated in GC and normal adjacent tissues of 80 patients using immunohistochemistry staining. The expression of Tensin4 mRNA was analyzed in 10 GC tissues and 3 GC cell lines (SGC7901, MKN45, and MKN28) by qPCR. Cell proliferation, migration, and invasion were assessed using CCK-8 and Transwell assays in the Tensin 4 siRNA transfected SGC7901 cells and Tensin 4 plasmid transfected MKN28 cells. Additionally, protein expressions of Tensin 4, E-cadherin, vimentin, AKT, p-AKT, GSK-3β, p-GSK-3β, and Snail were analyzed by western blotting. The results demonstrated that the expression of Tensin 4 was significantly up-regulated in the GC tissues and cell lines, especially in the SGC7901 cells. The expression of Tensin 4 positively correlated with p-AKT in GC tissues and with GC progression, and was an independent risk factor for the prognosis of GC. Tensin 4 promoted the invasion and migration abilities of GC cells, but had no significant effect on GC cell proliferation. Tensin 4 promoted the occurrence of epithelial mesenchymal transition (EMT) through up-regulating the expression of p-AKT, p-GSK-3β, and snail. Overall, this study suggests that the activation of AKT/GSK-3β/Snail signaling pathway promoted by Tensin 4 plays an important role in the progression of GC. Therefore, Tensin 4 may serve as a potential target in GC treatment.