Abstract
Neuroblastoma is a primary malignancy mainly occurring in children. We have reported that polymorphisms of several N6-methyladenosine (m6A) RNA modification-related genes contributed to neuroblastoma risk in previous studies. YTHDF2, a “reader” of RNA m6A modification, is involved in cancer progression. Here, we estimated the association between a YTHDF2 gene rs3738067 A>G polymorphism and neuroblastoma susceptibility in 898 neuroblastoma patients and 1,734 healthy individuals from China. We found that the rs3738067 A>G could decrease neuroblastoma risk [AG vs. AA: adjusted odds ratio (OR) = 0.76, 95% confidence interval (CI) = 0.64–0.90, P = 0.002; AG/GG vs. AA: adjusted OR = 0.81, 95% CI = 0.69–0.95, P = 0.011). Besides, the rs3738067 AG/GG genotype was related to reduced neuroblastoma risk in the following subgroups: children aged 18 months and under, boys, patients with tumors originating from retroperitoneal, patients at clinical stage IV, and cases at clinical stages III plus IV. Importantly, false-positive report probability analysis proved our significant results worthy of close attention of. The expression quantitative trait locus analysis results revealed that the rs3738067 was associated with the expression of YTHDF2.
Highlights
Neuroblastoma is a prevalent malignancy originating from precursor cells of the sympathetic nervous system, and it mainly affects infants and children under 5 years of age [1]
Based on the results of the single-locus analysis, we found that the G carriers of the rs3738067 were associated with decreased neuroblastoma risk (AG vs. AA: adjusted OR = 0.76, 95% confidence intervals (CIs) = 0.64–0.90, P = 0.002; AG/GG vs. AA: adjusted OR = 0.81, 95% CI = 0.69–0.95, P = 0.011)
Though many genetic variants linking to neuroblastoma susceptibility have been recognized, further efforts are needed to fully understand this disease’s genetic landscape
Summary
Neuroblastoma is a prevalent malignancy originating from precursor cells of the sympathetic nervous system, and it mainly affects infants and children under 5 years of age [1]. Neuroblastoma with high aggressiveness often progresses quickly, leading to a disappointing prognosis and high recurrence rate. Some patients experience mild or no treatment exhibit spontaneous regression [2], more than half of patients with high-risk neuroblastoma die even with multimodality treatment [3]. Due to the complex nature of the disease, the pathogenesis of neuroblastoma is still far from clear. Increasing evidence suggests that the gradual accumulation of adverse genetic alterations leads to the transformation of normal cells to cancer cells [4]. It is essential to uncover the detrimental genetic changes in neuroblastoma to screen for highrisk individuals and explore potentially effective treatment
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