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Genetic polymorphisms of tumor necrosis factor receptor-associated factor 3 and their association with acute
Fadwa M Alkhulaifi1, Hana Hakami1, Jamilah Alshammari1
1Zoology Department, College of Sciences, King Saud University, Riyadh, Saudi Arabia.
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.
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