Abstract
BackgroundHepatoblastoma 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.MethodsWe 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.ResultsNo 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.ConclusionsThe data suggest that NRAS and KRAS polymorphisms are irrelevant to hepatoblastoma susceptibility among Chinese population.
Highlights
Hepatoblastoma, an embryonic tumor, accounts for about 80% of all childhood liver malignancies and 1% of all childhood malignancies [1, 2]
The data suggest that NRAS and KRAS polymorphisms are irrelevant to hepatoblastoma susceptibility among Chinese population
Association between hepatoblastoma risk and NRAS and KRAS polymorphisms Genotypes at the NRAS polymorphism rs2273267 A > T are listed in Table 1 for hepatoblastoma patients and controls, along with those at the KRAS polymorphisms rs12587 G > T, rs7973450 A > G, and rs7312175 G > A
Summary
Hepatoblastoma, an embryonic tumor, accounts for about 80% of all childhood liver malignancies and 1% of all childhood malignancies [1, 2]. The genetic disorders Beckwith–Wiedemann syndrome and familial adenomatous polyposis are closely associated with hepatoblastoma, suggesting that genetic factors may accelerate pathogenesis [2]. 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 play critical roles in tumorigenesis. There are few studies on the association between the RAS gene polymorphisms and risk of hepatoblastoma
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