Background & Aims: The impact of tumor size on account of the long-term survival results in gallbladder cancer (GBC) patients has been controversial. It is urgent necessary to identify the optimal cutoff value of tumor size in resected GBC, and we attempted to integrate tumor size with other prognostic factors into a prognostic nomogram to predict the cancer-specific survival (CSS) of GBC patients. Methods 1639 patients with resected GBC were extracted from the Surveillance, Epidemiology and End Results (SEER) database. X-tile program was used to identify the optimal cutoff value of tumor size. A nomogram including tumor size was established to predict 1-, 3- and 5-year CSS based on the independent risk factors chosen by univariate and multivariable cox analyses. The precision of the nomogram for predicting survival was validated with Harrell’s concordance index (C-index), calibration curves, and receiver operating characteristic curve (ROC) internally and externally. Results Patients with GBC were classified into 1–13 mm, 14–63 mm and 64 mm subgroup based on the optimal cutoff for tumor size in terms of CSS. The nomogram according to the independent factors was well calibrated and displayed better discrimination power than 7th Tumor-Node-Metastasis (TNM) stage systems. Conclusions The results demonstrated that increased tumor size is closely associated with the worse CSS. Our novel nomogram, which outperforms the conventional TNM staging system, showed satisfactory accuracy and clinically practicality for predicting the outcome of resected GBC patients.

Background CircRNAs have been reported to be related to hepatocellular carcinoma (HCC) development. Limited studies have revealed the expression profile of circRNAs in tumor and paratumour normal samples in HCC patients. Methods The expression of circRNAs, mRNA and miRNA was detected by Real-time PCR. An immunofluorescence assay was performed to detect the level of 5mC and 5hmC. Dual luciferase assay was used to confirm the interaction between miRNA and circRNA. CCK8, wound healing and transwell assays were used to check the viability, migration and invasion of HCC cells. Migration and invasion assays was used to confirm the metastasis in vivo. Results We found that circASPH was significantly increased in HCC tumor samples and that the level of circASPH was closely related to the overall survival (OS) of HCC patients. Mechanistically, circASPH could regulate the methylation of promoter and gene expression of Hydrocyanic Oxidase 2 (HAO2) to promote HCC progression by acting as a sponge for miR-370, which targeted the DNMT3b and increased the 5mC level. Conclusions Our study determined that circASPH could promote the methylation and expression of HAO2 and could be considered an important epigenetic regulator in HCC progression.