Objective: To investigate the impact of using a three-dimensional (3D) printed liver model for patient education. Methods: Children with hepatic tumours who were scheduled for hepatectomy were enrolled, and patient-specific 3D liver models were printed with photosensitive resin, based on computed tomography (CT) images. Before surgery, their parents received information regarding liver anatomy, physiology, tumour characteristics, planned surgery, and surgical risks using these CT images. Then, parents completed questionnaires regarding this information. Thereafter, 3D printed models of each patient were presented along with an explanation of the general printing process, and the same questionnaire was completed. The median number of correct responses in each category before and after the 3D printed model presentation was compared. Results: Seven children and their 14 parents were enrolled in the study. After the presentation of 3D printed models, parental understanding of basic liver anatomy and physiology, tumour characteristics, the planned surgical procedure, and surgical risks significantly improved. Parents demonstrated improvements in their understanding of basic liver anatomy by 26.4%, basic liver physiology by 23.6%, tumour characteristics by 21.4%, the planned surgical procedure by 31.4%, and surgical risks by 27.9%. Conclusions: Using 3D printed liver models improved parental education regarding the understanding of liver anatomy and physiology, tumour characteristics, surgical procedure, and associated surgical risks.

Background: Hepatoblastoma (HB) is the most common hepatic malignancy in children, accounting for approximately 80% of all childhood liver tumors. Previous genome-wide association studies (GWASs) have found that the LINC00673 rs11655237 C>T polymorphism is associated with the risk of several different adult cancers. However, the association between this polymorphism and HB susceptibility remains unclear. Methods: We analyzed the association between the LINC00673 rs11655237 C>T polymorphism and HB susceptibility in a hospital-based study of Chinese children. We enrolled 213 HB patients and 958 healthy controls with genotypes determined by TaqMan, and the strength of the association of interest was determined by calculating odds ratios (ORs) and 95% confidence intervals (CIs). Findings: We found a significant association between the LINC00673 rs11655237 C>T polymorphism and HB risk (CT/TT compared with CC: adjusted OR = 1.40, 95% CI = 1.04–1.88, p = 0.029). Furthermore, stratified analysis indicated that rs11655237 T allele carriers in the following subgroups were more likely to develop HB: children older than 17 months, males, and those with tumors of clinical stages III + IV. Interpretation: In conclusion, we confirmed that the LINC00673 rs11655237 C>T polymorphism may be associated with HB susceptibility. Prospective studies with larger sample sizes and patients of different ethnicities are needed to validate our findings.

Background: Neuroblastoma (NB) is one of the deadliest paediatric solid tumours due to its rapid proliferative characteristics. Amplified copies of MYCN are considered the most important marker for the prediction of tumour relapse and progression in NB, but they were only detected in 20–30% of NB patients, indicating there might be other oncogenes in the development of NB. The far upstream element binding protein 1 (FUBP1) was first identified as a transcriptional regulator of the proto-oncogene MYC. However, the expression and role of FUBP1 in NB have not been documented.Methods: FUBP1 expression was analysed from GEO database and verified by immunohistochemistry (IHC) and western blotting (WB) in NB tissues and cell lines. Cell proliferation and apoptosis were detected by Cell Counting Kit-8, Colony formation assay, EDU, TUNEL staining and flow cytometric analysis. Several glycolytic metabolites production was confirmed by ELISA and oxygen consuming rate (OCR). Luciferase assay, WB, chromatin immunoprecipitation (CHIP) were used to explore the mechanisms of the effect of FUBP1 on NB.Results: FUBP1 mRNA levels were increased along with the increase in International Neuroblastoma Staging System (INSS) stages. High expression of FUBP1 with low N-Myc expression accounted for 44.6% of NB patient samples (n = 65). In addition, FUBP1 protein levels were remarkably increased with NB malignancy in the NB tissue microarray (NB: n = 65; ganglioneuroblastoma:n = 31; ganglioneuroma:n = 27). Furthermore, FUBP1 expression was negatively correlated with patient survival rate but positively correlated with ki67 content. In vitro experiments showed that FUBP1 promotes NB cell proliferation and inhibits cell apoptosis via enhancing glycolysis and ATP production. Mechanistically, FUBP1 inhibited the degradation of HIF1α via downregulation of Von Hippel-Lindau (VHL), the E3 ligase for HIF1α, resulting in upregulation of lactate dehydrogenase isoform B (LDHB) expression to enhance glycolysis. Overexpressed or silenced N-Myc could not regulate FUBP1 or LDHB levels.Conclusions: Taken together, our findings demonstrate for the first time that elevated FUBP1 promotes NB glycolysis and growth by targeting HIF1α rather than N-Myc, suggesting that FUBP1 is a novel and powerful oncogene in the development of NB independent of N-Myc and may have potential in the diagnosis and treatment of NB.

Neuroblastoma, which accounts for approximately 10% of all pediatric cancer-related deaths, has become a therapeutic challenge and global burden attributed to poor outcomes and mortality rates of its high-risk form. Previous genome-wide association studies identified the LINC00673 rs11655237 C>T polymorphism to be associated with the susceptibility of several malignant tumors. However, the association between this polymorphism and neuroblastoma susceptibility is not clear. We genotyped LINC00673 rs11655237 C>T in 393 neuroblastoma patients in comparison with 812 age-, gender- and ethnic-matched healthy controls. We found a significant association between the LINC00673 rs11655237 C>T polymorphism and neuroblastoma risk (TT vs. CC: adjusted odds ratio [OR]=1.80, 95% confidence interval [CI]=1.06-3.06, P =0.029; TT/CT vs. CC: adjusted OR=1.31, 95% CI=1.02-1.67, P =0.033; and T vs. C: adjusted OR=1.29, 95% CI=1.06-1.58, P =0.013). Furthermore, stratified analysis indicated that the rs11655237 T allele carriers were associated with increased neuroblastoma risk for patients with tumor originating from the adrenal gland (adjusted OR=1.51, 95% CI=1.06-2.14, P =0.021) and International Neuroblastoma Staging System stage IV disease (adjusted OR=1.60, 95% CI=1.12-2.30, P =0.011). In conclusion, we verified that the LINC00673 rs11655237 C>T polymorphism might be associated with neuroblastoma susceptibility. Prospective studies with a large sample size and different ethnicities are needed to validate our findings.