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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. [ABSTRACT FROM AUTHOR]

Hepatoblastoma (HB) is the most common pediatric liver malignancy. Management of HB requires multidisciplinary efforts. The 5-year overall survival of this disease is about 80% in developed countries. Despite advances in the care of these patients, survival in recurrent or treatment-refractory disease is lower than 50%. This is due to more complex tumor biology, including hepatocellular carcinoma (HCC)-like mutations and expression of aggressive gene signatures leading to chemoresistance, vascular invasion, and metastatic spread. The current treatment protocols for pediatric liver cancer do not incorporate targeted therapies, and the ability to test these therapies is limited due to the inaccessibility of cell lines and mouse models. In this review, we discuss the current status of preclinical animal modeling in pediatric liver cancer, primarily HB. Although HB is a rare cancer, the research community has worked together to develop a range of interesting and relevant mouse models for diverse preclinical studies. [ABSTRACT FROM AUTHOR]

Background: Hepatoblastoma is the most common hepatic malignancy in children, accounting for approximately 80% of all childhood liver tumors. KRAS and NRAS, members of the RAS gene family, are closely linked to tumorigenesis, and are frequently mutated in a variety of malignancies. They may thus play critical roles in tumorigenesis. However, there are few studies on the association between the RAS gene polymorphisms and risk of hepatoblastoma. Methods: We investigated whether the polymorphisms at these genes are associated with hepatoblastoma susceptibility in a hospital-based study of 213 affected Chinese children and 958 cancer-free controls. Genotypes were determined by TaqMan assay, and association with hepatoblastoma risk was assessed based on odds ratios and 95% confidence intervals. Results: No significant differences were observed between patients and controls in terms of age and gender frequency. All NRAS and KRAS genotypes are in Hardy–Weinberg equilibrium in the entire study population. We did not observe any significant association between hepatoblastoma risk and polymorphisms at NRAS and KRAS. The association between selected polymorphisms and hepatoblastoma risk was assessed after stratification by age, gender, and clinical stage. However, no significant association was observed even after stratification by age, gender, and clinical stage. Conclusions: The data suggest that NRAS and KRAS polymorphisms are irrelevant to hepatoblastoma susceptibility among Chinese population. [ABSTRACT FROM AUTHOR]