Heterozygote AG variant of −596 A/G IL-6 gene polymorphism is a marker for cutaneous T-cell lymphoma (CTCL)

Vaškú, Julie Anna Bienertová; Vašků, Anna; Goldbergová, Monika Pávková; Vašků, Vladimı́r

doi:10.1016/j.clim.2004.08.010

Cited by 13 publications

(14 citation statements)

References 28 publications

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“…The IL-6 -174G/C and IRF4 rs12203592 polymorphisms had been implicated in skin cancer susceptibility. More and more studies have investigated the relationship of IL-6 -174G/C and IRF4 rs12203592 polymorphisms with skin cancer risk [22][23][24][25][26][27][28][29][30][31][32] ; however, the results are contradictory. To get a comprehensive conclusion, we searched the literature from PubMed and EMBASE databases and conducted meta-analysis.…”

Section: Discussionmentioning

confidence: 94%

“…15 Recently, numerous studies have examined the potential contribution of the IL-6 gene -174G/C and IRF4 rs12203592 polymorphism to skin cancer susceptibility, but these studies have produced diverse results. [22][23][24][25][26][27][28][29][30][31][32] Given that a single study may be too underpowered to provide reliable conclusion owing to relatively small sample size, we performed this meta-analysis to estimate the association between IL-6 gene -174G/C and IRF4 rs12203592 polymorphism and skin cancer susceptibility more precisely.…”

Section: Introductionmentioning

confidence: 99%

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Meta-analysis of the Correlation Between Interleukin-6 Promoter Polymorphism -174G/C and Interferon Regulatory Factor 4 rs12203592 Polymorphism With Skin Cancer Susceptibility

Cao²,

Liu³

et al. 2016

American Journal of Therapeutics

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Inflammation is a process whereby the immune system responds to a disease or injury. Chronic inflammation, however, has been linked to several types of cancers such as skin cancer. Molecular epidemiological studies were carried out in recent years evaluating interferon regulatory factor 4 (IRF4) rs12203592 and interleukin-6 (IL-6) gene -174G/C polymorphism associated with skin cancer risk for different groups of people. However, the results are still conflicting, not conclusive. We performed a meta-analysis to investigate the association between cancer susceptibility and IL-6 -174G/C (1130 cases and 1260 controls from 7 studies) and IRF4 rs12203592 polymorphisms (3879 cases and 6759 controls from 9 studies) in different inheritance models. We assess the strength of association of odds ratio (ORs), 95% confidence interval (CI). Overall, significantly elevated skin cancer risk was found when all studies were pooled into the meta-analysis of IL-6 -174G/C (For GC vs. GG: OR = 1.28, 95% CI, 1.06-1.54, I = 0, Pheterogeneity = 0.816; for CC/GC vs. GG: OR = 1.26, 95% CI, 1.05-1.50, I = 0, Pheterogeneity = 0.618). However, for IRF4 rs12203592 polymorphism, significantly increased risk of skin cancer was observed in TT versus CC (OR = 1.99, 95% CI, 1.30-3.07, I = 76.7%, Pheterogeneity < 0.001) and in recessive model (OR = 1.91, 95% CI, 1.31-2.77, I = 69.9%, Pheterogeneity < 0.001). This meta-analysis indicates that the IL-6 gene -174G/C and IRF4 rs12203592 polymorphisms may be associated with an increased skin cancer risk.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Meta-analysis of the Correlation Between Interleukin-6 Promoter Polymorphism -174G/C and Interferon Regulatory Factor 4 rs12203592 Polymorphism With Skin Cancer Susceptibility

Cao²,

Liu³

et al. 2016

American Journal of Therapeutics

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“…Examples of specific genes investigated include those encoding for tumor necrosis factor alpha [34] and other cytokines [35], the p53 protein [36], DNA repair proteins [37], biotransformation enzymes [38], intermediates of the folate metabolism pathway [39], human leukocyte antigens (HLA) [40], and transcriptional factors (Bcl6 [41]). However, no strong susceptibility loci have yet been confirmed.…”

Section: Other Genetic Factorsmentioning

confidence: 99%

Epidemiology and etiology of non-Hodgkin lymphoma – a review

2006

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The etiology of non-Hodgkin lymphoma, as well as its global dramatic rise in incidence during the past decades, remains largely unexplained. However, there is increasing awareness that this group of malignancies may entail not only clinical, morphological and molecular heterogeneity, but also considerable variations in terms of etiologic factors. In this review, epidemiologic patterns are summarized as well as current evidence of associations between various known or suspected risk factors for non-Hodgkin lymphoma overall or for any of its subtypes. Central pathogenetic mechanisms include immunosuppression, especially in relation to T-cell function and loss of control of latent EBV infection, and chronic antigen stimulation. Some degree of familiar aggregation also implies a role for genetic susceptibility. A number of recent investigations of non-Hodgkin lymphoma etiology will hopefully lead to a better understanding of the causes of these malignancies.

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“…The IL-6 -174G/C polymorphism that we have studied in CTCL has already been proved to be related to inflammatory and autoimmune diseases [32][33][34]. Data including IL-6 polymorphisms in CTCL are rather limited and conflicting; however, the heterozygote variant of − 596 A/G promoter IL-6 polymorphism has been suggested a genotype marker for CTCL [35]. On the other hand, deregulation of STAT signaling plays a key role in pathogenesis of CTCL.…”

Section: Discussionmentioning

confidence: 98%

The polymorphisms of IL-6/STAT3 signaling pathway may contribute to cutaneous T-cell lymphomas susceptibility

et al. 2020

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IL-6/STAT3 signaling pathway has been suggested to play a role in CTCL pathogenesis. Polymorphisms in STAT3 signaling pathway-related genes might be a risk factor for CTCL. However, the exact role of inherited gene polymorphisms of IL-6 and STAT3 in the pathogenesis of CTCL is still not fully understood. The aim was to examine whether IL-6 cytokine and polymorphisms of IL-6 and STAT3 gene are associated with CTCL susceptibility, stage of disease and pruritus intensity. We compared the IL-6 serum level and the frequency of selected single nucleotide polymorphisms of IL-6 and STAT3 in 106 CTCL and 198 control group using polymerase chain reaction with sequence-specific primers method and ELISA. We have found that serum IL-6 level in CTCL patients was significantly higher than in healthy controls (p < 0.05). We also demonstrated that two genotypes, CC of IL-6 and GG of STAT3, were overexpressed in CTCL patients compared to healthy controls, and that they increase the risk of malignancy development (OR = 1.8, p = 0.04 for IL-6 and OR 2.53, p = 0.0064 for STAT3). Moreover, the GG genotype of STAT3 polymorphism seems to be associated with lack of pruritus or mild pruritus in CTCL patients. Our results indicate that IL-6 is involved in pathogenesis of CTCL but not pruritus. Moreover, CC of IL-6 and GG genotype of STAT3 genes might be considered as the risk factor for development of CTCL.

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Heterozygote AG variant of −596 A/G IL-6 gene polymorphism is a marker for cutaneous T-cell lymphoma (CTCL)

Cited by 13 publications

References 28 publications

Meta-analysis of the Correlation Between Interleukin-6 Promoter Polymorphism -174G/C and Interferon Regulatory Factor 4 rs12203592 Polymorphism With Skin Cancer Susceptibility

Meta-analysis of the Correlation Between Interleukin-6 Promoter Polymorphism -174G/C and Interferon Regulatory Factor 4 rs12203592 Polymorphism With Skin Cancer Susceptibility

Epidemiology and etiology of non-Hodgkin lymphoma – a review

The polymorphisms of IL-6/STAT3 signaling pathway may contribute to cutaneous T-cell lymphomas susceptibility

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