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Association of interleukin-6 genetic polymorphisms with risk of OSCC in Indian population

Interleukin-6 (IL-6) encodes a cytokine protein, which causes inflammation, maintains immune homeostasis and plays an essential role in oral pathogenesis. The aim of this study was to evaluate the association between IL-6 (−174 and −572) G/C promoter gene polymorphisms and risk of OSCC among Indians...

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Bibliographic Details
Published in:Meta Gene 2015-06, Vol.4, p.142-151
Main Authors: Singh, Prithvi Kumar, Chandra, Girish, Bogra, Jaishri, Gupta, Rajni, Kumar, Vijay, Jain, Amita, Hussain, Syed Rizwan, Mahdi, Abbas Ali, Ahmad, Mohammad Kaleem
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Language:English
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Summary:Interleukin-6 (IL-6) encodes a cytokine protein, which causes inflammation, maintains immune homeostasis and plays an essential role in oral pathogenesis. The aim of this study was to evaluate the association between IL-6 (−174 and −572) G/C promoter gene polymorphisms and risk of OSCC among Indians. Single nucleotide polymorphism in IL-6 genes was genotyped in OSCC patients and healthy controls by PCR-RFLP method. Genotype and allele frequencies were analyzed by chi-square test and strength of associations by odds ratio with 95% confidence intervals. Frequency distribution of IL-6 (−174) G/C gene polymorphism was significantly associated with OSCC patients in comparison to healthy controls (OR: 0.541, CI: 0.356–0.822; p: 0.004. However, frequency of IL-6 (−572) G/C gene polymorphism was not significantly associated with OSCC patients (p>0.05). The genotype GC and allele C of IL-6 (−174) G/C gene polymorphism play a significant role in OSCC susceptibility. •We first demonstrate the IL-6 polymorphism in OSCC patients in Indian population.•We obtained the SNP of IL-6 (-174) is increase the risk of OSCC.•We also obtained the SNP of IL-6 (-572) and risk of OSCC•We evaluate the correlation of these IL-6 polymorphisms and progression of OSCC.•We identified the environmental factors and gene interactions with pathogenesis of OSCC.
ISSN:2214-5400
2214-5400
DOI:10.1016/j.mgene.2015.03.002