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Purpose: The explosive progression of residual hepatocellular carcinoma (HCC) following incomplete thermal ablation is challenging, and the underlying mechanisms require further exploration. We investigated the mechanism by which Forkhead box P4 (FOXP4) promotes the malignant transformation of residual HCC cells through N-deacetylase and N-sulfotransferase 2 (NDST2) after incomplete thermal ablation. Methods: The clinical significance of FOXP4 and NDST2 in HCC was evaluated using big data analysis. FOXP4 expression was detected in clinical samples of HCC. The gene expression levels in an in vitro heat-stressed HCC cell model were determined using quantitative real-time PCR (RT-qPCR) and Western blotting. The effects of the genes on heat-stressed HCC cells were investigated using Cell Counting Kit-8 (CCK-8), scratch, Transwell migration, and invasion assays. Additionally, the regulatory relationship between FOXP4 and NDST2 was validated using the Cleavage Under Targets and Tagmentation (CUT&Tag) experiments and phenotypic assays. Results: High FOXP4 expression was correlated with liver cancer occurrence and development. In the heat-stressed HCC cell model, downregulating FOXP4 inhibited cancer cell progression. Besides, there was a positive association between FOXP4 and NDST2 in liver cancer. Suppressing FOXP4 reduced NDST2 expression in the heat-stressed HCC cells. Furthermore, reducing NDST2 expression weakened the biological behavior of heat-stressed HCC cells. Conclusion: FOXP4 and NDST2 are crucial in the incomplete thermal ablation of residual cancer. FOXP4 might regulate the biological progression of residual HCC after incomplete thermal ablation through NDST2. [ABSTRACT FROM AUTHOR]

Objectives: The present study aimed to determine the feasibility of the American College of Radiology's (ACR) contrast‐enhanced ultrasound (CEUS) Liver Imaging Reporting and Data System (LI‐RADS) (version 2017) in examinations using Sonazoid and compare its diagnostic performance with that of modified LI‐RADS in patients at high risk of hepatocellular carcinoma (HCC). Methods: This retrospective study's sample population consisted of 137 participants with a total of 140 nodules who underwent CEUS with Sonazoid and pathological confirmation via surgery or biopsy from January 2020 to February 2022. The lesions were evaluated and classified based on the reference standards (ie, ACR CEUS LI‐RADS and modified LI‐RADS). The overall diagnostic capabilities of the two systems were evaluated in terms of accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) with 95% confidence intervals (CIs). Results: The participants had a median age of 51 years and an interquartile range of 43–58 years. Regarding LR‐5 as a predictor of HCC, the accuracy results of the ACR LI‐RADS and modified LI‐RADS algorithms were 72.9 and 71.4%, respectively (P =.50). The sensitivity of both systems was the same (69.7%; 95% CI: 60.7–77.8%). Regarding LR‐M as a predictor of non‐HCC malignancy, the diagnostic performance of the algorithms was the same, with accuracy and sensitivity results of 76.4 and 73.3%, respectively (95% CI: 44.9–92.2%). Conclusion: The findings indicate that modified LI‐RADS had a moderate level of diagnostic performance for HCC in examinations using Sonazoid, which was comparable to ACR LI‐RADS. [ABSTRACT FROM AUTHOR]

Background: The mechanism of microRNAs (miRNAs) in thyroid cancer is still unclear. We identified miRNAs with differential expression in thyroid cancer versus normal tissues., Methods: Microarray datasets were obtained from the GEO and ArrayExpress databases, and from publications found via PubMed, EMBASE, and Web of Science. Differentially expressed miRNAs were identified using the limma package, and their targets predicted using miRWalk. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) network analyses were performed using these target genes to explore potential carcinogenic mechanisms. Correlations between target gene and miRNA expression levels were examined. Changes in target protein expression were confirmed using data from The Human Protein Atlas and the Cancer Genome Atlas., Results: We ultimately included five datasets, and further analyzed the four miRNAs that were down-regulated in at least four datasets (miR-7-2-3p, miR-138-5p, miR-144-5p, miR-486-5p). Predicted targets were enriched in GO terms including extracellular matrix organization, cell surface, and receptor binding, and in KEGG cancer pathways. PPI analysis identified 10 hub genes as key potential targets of these miRNAs. The expression levels of eight target genes were negatively correlated with those of their respective miRNAs. Furthermore, eight predicted target genes in cancer-related pathways showed up-regulated protein and mRNA expression in thyroid cancer., Conclusion: Low miRNA expression in thyroid cancer might influence tumorigenesis via critical pathways. The genes identified here may act as a starting point for further investigation of the carcinogenic mechanisms of these miRNAs., Competing Interests: None.