The aim of this study was to explore the association between polymorphisms of five cytokine genes and clinical parameters in patients with Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) treated with imatinib. We analyzed five cytokine genes (interleukin [IL]-6, IL-10, gamma interferon [IFN-γ], transforming growth factor beta-1 [TGF-β1], and tumor necrosis factor-alpha [TNF-α]) in 60 cases with Ph+ CML and 74 healthy controls. Cytokine genotyping was performed by the polymerase chain reaction-sequence-specific primer. All data were analyzed using the de Finetti program and SPSS version 14.0 for Windows. No significant differences were detected between the CML group and healthy controls with respect to the distributions and numbers of genotypes and alleles in TNF-α, TGF-β1, IL-10, and IFN-γ. However, the GG genotype associated with high expression in IL-6 was found to be significantly more frequent in CML as compared to controls (p=0.010). The median follow-up time was 49.3 months (range 6.1-168.4) and the median duration of imatinib treatment was 39.5 months (range 5.2-103.4) for these patients. On multivariateanalysis, only IL-10 GCC/GCC highly produced haplotypes were significantly associated with a shorter event-free survival. The relationship between cytokine genotypes/haplotypes and clinical parameters in CML has not been investigated before. Our results suggest that IL-10 may be a useful marker for CML prognosis and theGG genotype of the IL-6 gene may be associated with susceptibility.
Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by the accumulation of fat in the liver, progressing from simple steatosis to various complications, with increasing prevalence in the modern world. Our study aimed to investigate the relationship between MASLD pathogenesis and the presence of apolipoprotein C-III (ApoC-III) gene variants rs2854116 and rs2854117 by comparing allele and genotype frequencies between MASLD patients and healthy individuals, as well as analyzing their association with biochemical parameters in Turkish populations. Materials and Methods: The study included 202 MASLD patients and 100 healthy controls who presented to our outpatient clinic. MASLD presence was determined by ultrasonography (USG). The demographic, laboratory, and clinical data of the participants were recorded. ApoC-III gene variants rs2854116 and rs2854117 were genotyped using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method from genomic DNA samples obtained from blood. Results: The genotype and allele frequencies of ApoC-III gene variants rs2854116 and rs2854117 did not show significant differences between patient and healthy groups (p > 0.05). When biochemical parameters were evaluated, the LDH value of rs2854116 variant CT/CC genotype carriers was found to be significantly higher than TT genotype carriers (p = 0.016). Conclusions: We observed a high prevalence of MASLD in our Turkish cohort. However, the specific genetic variants we investigated were not associated with MASLD status. This suggests that these variants may not be significant contributing factors to MASLD in this population.