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• W2951802839 abstract "Abstract Background While leukocyte telomere length has been linked with altered risk in adult cancer, limited information is available on its association with risk in pediatric solid tumors. We investigated the association of telomeric alterations with risk of pediatric solid tumors. We also investigated whether altered telomeres cooperated with the TP 53 rs1042522, MDM 2 rs2279744 and CDKN 1A (p21 cip1 ) rs1059234 single‐nucleotide polymorphisms to modify cancer risk. Methods A total of 101 tumor patients and 202 controls were recruited for this age‐ and gender‐matched case–control study. Relative telomere length ( RTL ) was determined in peripheral blood leukocytes using quantitative real‐time polymerase chain reaction ( PCR ), and the polymorphisms were genotyped using PCR –restriction fragment length polymorphism. Results Using median RTL in the healthy controls as a cut‐off, children with longer telomeres were at an increased risk of developing a solid tumor ( OR , 2.70; P < 0.01). When participants were categorized according to control RTL quartiles, a significant dose–response relationship was observed (χ 2 = 10.95; P < 0.001). The risk for tumors increased nearly threefold ( P = 0.001) for the triple interaction RTL × TP 53 rs1042522 × p21 cip1 rs1059234 compared with the maximum effect of any single factor, although the interaction effect was less than additive. The MDM 2 rs2279744 GG genotype reduced pediatric solid tumor risk significantly ( OR , 0.51). Conclusion Combined analysis of telomeres and genetic polymorphisms in the TP 53 pathway can provide important clues to understanding pediatric solid tumor etiology." @default.
• W2951802839 created "2019-06-27" @default.
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• W2951802839 date "2019-08-01" @default.
• W2951802839 modified "2023-09-26" @default.
• W2951802839 title "Long telomeres cooperate with p53 , MDM 2 , and p21 polymorphisms to raise pediatric solid tumor risk" @default.
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• W2951802839 doi "https://doi.org/10.1111/ped.13915" @default.
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