Cytokine gene polymorphisms in Turkish patients with chronic myeloid leukaemia and in healthy controls Kroni̇k mi̇yeloi̇d lösemi̇li̇ hastalar ve saǧlikli kontrollerde si̇toki̇n gen poli̇morfi̇zmi̇

ÖZDİLLİ K., PEHLİVAN S., Öret Y. D., Sever T., Pehlivan M., İŞSEVER H., ...Daha Fazla

Nobel Medicus, cilt.10, sa.1, ss.74-78, 2014 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 10 Sayı: 1
  • Basım Tarihi: 2014
  • Dergi Adı: Nobel Medicus
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.74-78
  • Anahtar Kelimeler: Chronic myeloid leukemia, Cytokine gene polymorphism, IL-6, TNF-α
  • İstanbul Medipol Üniversitesi Adresli: Hayır

Özet

Objective: Cytokines that are released from activated lymphocytes, monocytes, and macrophages modify the intensity of immune inflammatory responses. Differences in cytokine production are due to sequence variants in cytokine genes. Cytokines are involved in all biological processes related to cell growth, cell differentiation, inflammation, and immunity. Early studies have demonstrated individual differences in cytokine production and an association between higher or lower cytokine production and disease. Chronic myelogenous leukaemia (CML) is a haematological malignancy that arises in haematopoietic stem cells with lymphoid and myeloid differentiation. Several studies have investigated the role of human leukocyte antigen (HLA) and cytokine gene polymorphisms in CML. The aim of this study was to analyse the role of cytokine polymorphisms in the aetiopathogenesis of CML. The susceptibility and protection of cytokine polymorphisms were evaluated. Material and Method: A total of 300 adult healthy controls and 85 (70 adult and 15 paediatric) patients who were diagnosed with chronic-phase philadelphia chromosome (Ph)+ CML were included in this study. The typing was performed using the polymerase chain reaction-sequence specific primer (PCR-SSP) method. The allele and genotype frequencies of the following cytokine genes were determined: interleukin (IL)-6 (-174 G/C), IL-10 (-1082 G/A, -819 T/C, and -592 A/C), interferon-gamma (IFN-g) (+874 A/T), transforming growth factor-beta (TGF-β) (C/T codon 10, C/G codon 25), and tumor necrosis factor- alpha (TNF-α) (-308 G/A). Results: We found that the frequencies of the TNF-α GA and IL-6 GC genotypes were higher in the healthy controls, and the differences between the CML patients and the controls were statistically significant. The analysis of the allele frequencies did not reveal statistically significant differences between the controls and the CML patients at 8 loci. Conclusion: The TNF-α GA and IL-6 GC genotypes may be protective alleles in CML patients.