title: The Associations of IL-6, IFN-γ, TNF-α, IL-10, and TGF-β1 Functional Variants with Acute Myeloid Leukemia in Turkish Patients.
abstract: OBJECTIVE
  It has been suggested that cytokine dysregulation could be associated with pathogenesis, progression, and survival in acute myeloid leukemia (AML). The purpose of this study was to evaluate the relationship of functional single-nucleotide polymorphisms (SNPs) in cytokine gene and cytokine expression levels with AML.
  
  
  METHODS
  Peripheral blood samples were collected from 42 patients with AML and 85 healthy individuals. Eight SNPs in five cytokine genes, including interleukin 6 (IL-6), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and transforming growth factor-β 1 (TGF-β1), were analyzed using the polymerase chain reaction sequence-specific primer method.
  
  
  RESULTS
  We found that the frequencies of the TNF-α (-308) GG genotype and G allele were significantly higher in the patients with AML compared to the healthy control group (p = 0.020 and 0.014). The AML patients had significantly lower frequencies of the CC genotype and C allele of the IL-10 (-819 SNP), the G allele of the IL-10 (-1082 SNP), the CC genotype and C allele of the IL-10 (-592 SNP), and the codon 25 GC genotype of TGF-β1, (p = 0.024, p = 0.012, p = 0.038, p = 0.024, p = 0.012, p = 0.028, respectively). However, no significant differences were found between AML and healthy control groups with respect to the distributions of genotypes in IL-6, IFN-γ, IL-10 (-1082), TGF-β1 (codon 10), and haplotypes of IL-10, TGF-β1 gene.
  
  
  CONCLUSIONS
  Our results suggest that functional variants of the TNF-α, IL-10, and TGF-β1 genes may have a significant association with the etiopathogenesis of AML. Further studies with larger groups and different ethnicities are needed to determine the impact of cytokine variants on the risk of developing AML.
authors.affiliation: 1 Department of Medical Genetics, Faculty of Medicine, Giresun University , Giresun, Turkey .
authors.forename: Ayse Feyda
authors.initials: AF
authors.lastname: Nursal
authors.affiliation: 2 Department of Hematology, Faculty of Medicine, Gaziantep University , Gaziantep, Turkey .
authors.forename: Mustafa
authors.initials: M
authors.lastname: Pehlivan
authors.affiliation: 2 Department of Hematology, Faculty of Medicine, Gaziantep University , Gaziantep, Turkey .
authors.forename: Handan Haydaroğlu
authors.initials: HH
authors.lastname: Sahin
authors.affiliation: 3 Department of Medical Biology, Istanbul Medical Faculty, Istanbul University , Istanbul, Turkey .
authors.forename: Sacide
authors.initials: S
authors.lastname: Pehlivan
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D016022:Case-Control Studies; D003062:Codon; D005260:Female; D005787:Gene Frequency; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics*; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics*; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics*; D015470:Leukemia, Myeloid, Acute / Q000097:blood / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics*; D014421:Turkey
chemical_list: D003062:Codon; C508609:IL10 protein, human; D015850:Interleukin-6; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma