International journal of hepatology · 2026
Association of the STAT3 rs1053004 Polymorphism With Hepatocellular Carcinoma in Iraqi Patients With Hepatitis B.
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Ali Hawraa Ahmed, Habeeb Thuraya Aamer, Shaker Zahraa F, Jasim Zahraa Q
Аннотация
INTRODUCTION: HCC is still one of the main causes of cancer-related fatalities despite years of intensive attempts to prevent it. One known risk factor is a persistent hepatitis B virus (HBV) infection. Previous studies have indicated a contribution of the STAT3 signaling pathway to carcinogenesis through inflammation mechanisms. In this study, we tried to explore the correlation between STAT3 rs1053004 polymorphism and HCC occurrence in people with HBV infection in Iraq.
METHODS: A case-control approach was applied with the inclusion of 80 patients with HCC due to HBV infection, 80 patients with CHB, and 80 healthy controls. The study was based on genotyping of the STAT3 rs1053004 polymorphism by a TaqMan SNP genotyping assay. Multivariate logistic regression analysis was used to assess the genetic association with disease risk, adjusting for potential confounding factors.
RESULTS: The three groups under study had significantly different genotype and allele distributions (p < 0.001). The HCC group had more T alleles than the other groups. Additionally, patients with the TT genotype had a greater risk of HCC (adjusted odds ratio [AOR] = 4.26; 95%confidence interval [CI] = 1.89-9.62; p < 0.001), and this impact was observed in patients with cirrhosis, high serum HBV DNA levels, and negative HBeAg status.
CONCLUSION: STAT3 rs1053004 polymorphism plays a significant role in the development of HCC risk in people with HBV infection.
METHODS: A case-control approach was applied with the inclusion of 80 patients with HCC due to HBV infection, 80 patients with CHB, and 80 healthy controls. The study was based on genotyping of the STAT3 rs1053004 polymorphism by a TaqMan SNP genotyping assay. Multivariate logistic regression analysis was used to assess the genetic association with disease risk, adjusting for potential confounding factors.
RESULTS: The three groups under study had significantly different genotype and allele distributions (p < 0.001). The HCC group had more T alleles than the other groups. Additionally, patients with the TT genotype had a greater risk of HCC (adjusted odds ratio [AOR] = 4.26; 95%confidence interval [CI] = 1.89-9.62; p < 0.001), and this impact was observed in patients with cirrhosis, high serum HBV DNA levels, and negative HBeAg status.
CONCLUSION: STAT3 rs1053004 polymorphism plays a significant role in the development of HCC risk in people with HBV infection.