No abstract

Objective. To explore the application value of the radiomics method based on enhanced T1WI in glioma grading. Materials and Methods. A retrospective analysis was performed using data of 114 patients with glioma, which was confirmed using surgery and pathological tests, at our hospital between January 2017 and November 2020. The patients were randomly divided into the training and test groups in a ratio of 7 : 3. The Analysis Kit (AK) software was used for radiomic analysis, and a total of 461 tumor texture features were extracted. Spearman correlation analysis and the least absolute shrinkage and selection (LASSO) algorithm were employed to perform feature dimensionality reduction on the training group. A radiomics model was then constructed for glioma grading, and the validation group was used for verification. Results. The area under the ROC curve (AUC) of the proposed model was calculated to identify its performance in the training group, which was 0.95 (95% CI = 0.905–0.994), accuracy was 84.8%, sensitivity was 100%, and specificity was 77.8%. The AUC of the validation group was 0.952 (95% CI = 0.871–1.000), accuracy was 93.9%, sensitivity was 90.0%, and specificity was 95.6%. Conclusions. The radiomics model based on enhanced T1WI improved the accuracy of glioma grading and better assisted clinical decision-making.

Gastric cancer is the third most commonly cause of tumor-related death worldwide and one of the most prevalent malignancies in China. TCL1A, TCL1 family Akt coactivator A, can active Akt/mTOR pathway and regulate the autophagy. However, the action of TCL1A in gastric cancer is not well understood. The present study is investigating the mechanism of action of TCL1A in gastric cancer. TCL1A was lowly expressed in gastric cancer tissues. Subsequent experiments demonstrated that miR-181a-5p can regulate c-MYC through the TCL1A-Akt/mTOR pathway and c-MYC can in turn affect the expression of miR-181a-5p, thus confirming the existence of the miR-181a-5p-TCL1A-Akt/mTOR-c-MYC loop. Flow cytometric apoptosis assay and mRFP-eGFP-LC3 autophagy assay demonstrated that both miR-181a-5p and TCL1A can affect autophagy and apoptosis of gastric cancer cells through the loop. In vivo experiments confirmed that TCL1A can affect the proliferation of gastric cancer. These results illustrate that TCL1A can exert tumour suppressive effects and affect gastric cancer autophagy and progression via the miR-181a-5p-TCL1A-Akt/mTOR-c-MYC loop, which could be a potential therapeutic target for gastric cancer.

No abstract

No abstract