Tumor necrosis factor a (TNFa) is an inflammatory cytokine that plays a crucial role in the immune response and the progression of cervical lesions. There is a growing body of data evaluating the value of a genetic variant in the TNFa gene with the risk of developing cervical cancer. The aim of this study was to explore the association of a variant, TNF‐308 G>A, residing in the TNFa gene with cervical cancer. A total of 91 women with cervical cancer and 161 women as the control group were recruited. DNA was extracted, and Taqman®‐probes‐based assay was used for genotyping. Our results showed that the minor allele frequency was 0.3 in total population, and the frequency of minor allele A was more in the case group compared with the control. The regression models in different genetic models also revealed that the allele A is a potential risk factor for the development of cervical cancer. In particular, in the dominant model, patients with AG and AA genotypes had a higher risk of developing cervical cancer with odds ratio (OR) of 2.75 (95% confidence interval [CI]: 1.57‐4.83, <0.001) and OR of 7.27 (95%CI: 2.5‐20.8, <0.001), compared with the GG genotype. Moreover, a similar outcome was obtained for smear test results. Our study demonstrated that TNF‐308 G>A located on TNF‐a was associated with the risk of cervical cancer, supporting further studies in a larger population and multicenter setting to show the value of emerging markers as risk stratification biomarkers in cervical cancer.

Our findings suggest a relationship between the CYP1B1-rs1056836 genetic polymorphism and clinical features of ESCC, supporting further studies in larger populations in different ethnic groups, taking into account potentially important environmental factors such as diet.

Background: Heat shock protein 27 (HSP27) is an intracellular chaperone constitutively expressed in many cell types including cardio myocytes and endothelial cells. Circulating levels of HSP27 and anti-HSP27 antibody are higher in patients with CVD. Anti-HSP27 antibody concentrations were also reported to be increased in atherogenesis. We aimed to evaluate serum anti-HSP27 antibody titers in individuals with, or without, MetS in the MASHAD study cohort with large sample size in 6,568 subjects. Methods: Participants with MetS were identified from MASHAD cohort (n=3358) using the IDF criteria, and the control group were those individuals who did not meet these criteria (n=3210). In-house enzyme-linked immune sorbent assay (ELISA) method was used for measuring Anti-HSP27 antibody levels. The two groups were matched for age, sex and smoking habit. Results: As expected, there were significant differences in height (p= 0.004), waist and hip circumference, weight, BMI, systolic and diastolic blood pressure, TGs, TC, HDL-C, Hs-CRP, glucose, with the presence of diabetes mellitus, hypertension, hyperlipidemia (p<0.001) between the two groups. Serum HSP27 antibody titers did not show significant difference between the groups with and without metabolic syndrome (p= 0.740). Conclusion: In conclusion, our results revealed serum anti-HSP27 antibody titers were not statistically different between individuals with and without MetS. However, it is possible that drug treatment may affect antibody titers and confound our findings in this population sample..

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