Genetic polymorphisms of tumor necrosis factor receptor-associated factor 3 and their association with acute lymphoblastic leukemia.
[BACKGROUND] Acute lymphoblastic leukemia (ALL) is an aggressive hematological malignancy driven by genetic and immunological dysregulation.
- p-value p < 0.05
- 연구 설계 case-control
APA
Alkhulaifi FM, Hakami H, et al. (2026). Genetic polymorphisms of tumor necrosis factor receptor-associated factor 3 and their association with acute lymphoblastic leukemia.. Cancer genetics, 302-303, 112-115. https://doi.org/10.1016/j.cancergen.2026.01.012
MLA
Alkhulaifi FM, et al.. "Genetic polymorphisms of tumor necrosis factor receptor-associated factor 3 and their association with acute lymphoblastic leukemia.." Cancer genetics, vol. 302-303, 2026, pp. 112-115.
PMID
41619431
Abstract
[BACKGROUND] Acute lymphoblastic leukemia (ALL) is an aggressive hematological malignancy driven by genetic and immunological dysregulation. Tumor necrosis factor receptor-associated factor 3 (TRAF3) plays an essential role in regulating immune signaling, lymphocyte homeostasis, and NF-κB pathways. Although TRAF3 alterations have been implicated in various immune disorders and hematologic cancers, the contribution of TRAF3 genetic polymorphisms to ALL susceptibility remains insufficiently understood.
[PURPOSE] To investigate the association between three TRAF3 single nucleotide polymorphisms (SNPs); rs33980500, rs13210247, and rs1131877, and ALL susceptibility in Saudi patients, and to evaluate TRAF3 mRNA expression levels in ALL compared to healthy individuals.
[METHODS] A case-control study was conducted involving 150 newly diagnosed ALL patients and 115 age- and sex-matched healthy controls. Genotyping of the selected TRAF3 SNPs was performed using TaqMan allelic discrimination assays. TRAF3 mRNA expression in peripheral blood white cells was quantified through RT-qPCR. Statistical analyses included genotype/allele frequency comparisons, odds ratios, Hardy-Weinberg equilibrium testing, linkage disequilibrium assessment, and haplotype construction.
[RESULTS] None of the analyzed SNPs showed a statistically significant association with ALL across genotype, allele, or haplotype models. Linkage disequilibrium between the SNPs was absent. However, TRAF3 mRNA expression was significantly upregulated in ALL patients, exhibiting a 3.88-fold increase compared with controls (p < 0.05).
[CONCLUSION] Although the examined TRAF3 SNPs were not associated with ALL susceptibility in this cohort, the marked elevation of TRAF3 mRNA expression suggests a potential role for TRAF3-related signaling in ALL pathogenesis. TRAF3 expression may represent a promising biomarker warranting further investigation.
[PURPOSE] To investigate the association between three TRAF3 single nucleotide polymorphisms (SNPs); rs33980500, rs13210247, and rs1131877, and ALL susceptibility in Saudi patients, and to evaluate TRAF3 mRNA expression levels in ALL compared to healthy individuals.
[METHODS] A case-control study was conducted involving 150 newly diagnosed ALL patients and 115 age- and sex-matched healthy controls. Genotyping of the selected TRAF3 SNPs was performed using TaqMan allelic discrimination assays. TRAF3 mRNA expression in peripheral blood white cells was quantified through RT-qPCR. Statistical analyses included genotype/allele frequency comparisons, odds ratios, Hardy-Weinberg equilibrium testing, linkage disequilibrium assessment, and haplotype construction.
[RESULTS] None of the analyzed SNPs showed a statistically significant association with ALL across genotype, allele, or haplotype models. Linkage disequilibrium between the SNPs was absent. However, TRAF3 mRNA expression was significantly upregulated in ALL patients, exhibiting a 3.88-fold increase compared with controls (p < 0.05).
[CONCLUSION] Although the examined TRAF3 SNPs were not associated with ALL susceptibility in this cohort, the marked elevation of TRAF3 mRNA expression suggests a potential role for TRAF3-related signaling in ALL pathogenesis. TRAF3 expression may represent a promising biomarker warranting further investigation.
MeSH Terms
Humans; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Polymorphism, Single Nucleotide; Male; Female; TNF Receptor-Associated Factor 3; Case-Control Studies; Genetic Predisposition to Disease; Adult; Child; Adolescent; Young Adult; Linkage Disequilibrium; Child, Preschool; Genotype; Haplotypes; Gene Frequency; Middle Aged; RNA, Messenger