Association between polymorphism of RAD50 gene and acute lymphoid leukemia in children

LI Wen; XU Zhi-Liang

doi:10.7499/j.issn.1008-8830.2015.05.011

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Chinese Journal of Contemporary Pediatrics ›› 2015, Vol. 17 ›› Issue (5) : 469-471. DOI: 10.7499/j.issn.1008-8830.2015.05.011

CLINICAL RESEARCH

Association between polymorphism of RAD50 gene and acute lymphoid leukemia in children

LI Wen, XU Zhi-Liang

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Abstract

Objective To investigate the association between single nucleotide polymorphism (SNP) (rs17166050) in RAD50 gene and acute lymphoid leukemia (ALL) in children. Methods A total of 177 ALL children from Wuhan and surrounding areas and 232 healthy children were selected. The numbers of standard-risk, medium-risk, and high-risk children were 66, 69, and 42, respectively. The genotypes of SNP in RAD50 gene were determined using PCR-RFLP, and the relationship of the RAD50 polymorphism with ALL susceptibility and clinical risk was analyzed. Results The genotype (AA, GA, and GG) distribution of SNP in RAD50 gene showed significant differences between the ALL and control groups (P=0.038), and G allele was significantly associated with ALL susceptibility (OR=1.459, 95% CI: 1.034-2.057, P=0.031). However, the SNP was not associated with the risk stratification of ALL. Conclusions The SNP (rs17166050) in RAD50 gene is associated with the susceptibility to ALL in children, but is not associated with the risk stratification of ALL.

Key words

Leukemia / RAD50 gene / Polymorphism / Risk / Child

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LI Wen, XU Zhi-Liang. Association between polymorphism of RAD50 gene and acute lymphoid leukemia in children[J]. Chinese Journal of Contemporary Pediatrics. 2015, 17(5): 469-471 https://doi.org/10.7499/j.issn.1008-8830.2015.05.011

References

[1] Pui CH, Relling MV, Downing JR, et al. Acute lymphoblastic leukemia[J]. N Engl J Med, 2004, 350(15): 1535-1548.
[2] Chatterton Z, Morenos L, Saffery R, et al. DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia[J]. Epigenomics, 2010, 2(5): 679-708.
[3] Williams GJ, Lees-Miller SP, Tainer JA. Mre11-Rad50-Nbs1 conformations and the control of sensing, signaling, and effector responses at DNA double-strand breaks[J]. DNA Repair (Amst), 2010, 9(12): 1299-1306.
[4] Kuroda S, Urata Y, Fujiwara T. Ataxia-telangiectasia mutated and the Mre11-Rad50-NBS1 complex: promising targets for radiosensitization[J]. Acta Med Okayama, 2012, 66(2): 83-92.
[5] Travis HS, John HJ. The MRE11 complex: starting from the ends[J]. Nat Rev Mol Cell Biol, 2011, 12(2): 90-103.
[6] Mosor M, Ziolkowska-Suchanek I, Nowicka K, et al. Germline variants in MRE11/RAD50/NBN complex genes in childhood leukemia[J]. BMC Cancer, 2013, 13: 457.
[7] 中华医学会儿科学会血液学组. 儿童急性淋巴细胞白血病诊疗建议（第三次修订草案）[J]. 中华儿科杂志, 2006, 44(5): 392-395.
[8] Berardineli F, di Masi A, Antoccia A. NBN gene polymorphisms and cancer susceptibility: a systemic review[J]. Curr Gemomics, 2013, 14(7): 425-440.
[9] Jackson SP, Bartek J. The DNA-damage response in human biology and disease[J]. Nature, 2009, 461(7267): 1071-1078.
[10] Onnie C, Fisher SA, King K, et al. Sequence variation, linkage disequilibrium and association with Crohn's disease on chromosome 5q31[J]. Genes Immun, 2006, 7(5): 359-365.
[11] Damiola F, Pertesi M, Oliver J, et al. Rare key functional domain missense substitutions in MRE11A, RAD50, and NBN contribute to breast cancer susceptibility: results from a Breast Cancer Family Registry case-control mutation-screening study[J]. Breast Cancer Res, 2014, 16(3): R58.