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Abstract
Hepatitis C virus (HCV) is a major global health care problem; it is the most common cause of chronic liver disease and cirrhosis, and the most common indication for liver transplantation worldwide. Chronic HCV infection is the main cause of liver cirrhosis and liver cancer in Egypt and, indeed, one of the top five leading causes of death. The risk of developing HCV- related HCC increases dramatically with the degree of hepatic fibrosis.
The risk of developing HCV-HCC may be magnified by the presence of concomitant factors. In HCV- infected persons, older patient age, male gender, obesity, steatosis, DM, liver disease severity, Asian or African-American race, heavy alcohol intake (> 50 g/d), hepatic iron deposition, co-infection with HBV, and co-infection with HIV have all been suggested to increase the risk of development of HCV-HCC.
Human cancer can be initiated by DNA damage caused by UVR, ionizing radiation, and environmental chemical agents. To safeguard the integrity of genome, humans have developed a set of complex DNA repair systems. The presence of inflammatory cells along with the production of inflammatory cytokines activates cellular oxidant-generating pathways. Reactive oxygen species released from inflammatory cells or induced by inflammatory cytokines are capable of producing a variety of different types of oxidative DNA lesions. Accumulation of reactive oxygen species, or repair of oxidative DNA lesions is a potential candidate to modify individual susceptibility to HCC. X-ray repair cross complementing group 1 (XRCC1), one of the more than 20 genes that participate in base excision repair pathway, encodes a scaffolding protein that functions in the repair of single-strand breaks, the most common lesions in cellular DNA.
Interleukin-1 (IL-1) is one of the most potent proinflammatory cytokines involved both in physiological immune responses and in the development of various immunopathological disorders. Interestingly, besides its major role as a proinflammatory cytokine, IL-1β has been implicated as an important factor for tumor growth. Several independent lines of evidence have also suggested that genetic polymorphisms within IL-1β gene are associated with gastric cancer and HCC in HCV infection.
Human genetic variation can modulate the risk of developing a cancer, the risk of developing symptoms related to cancer and its treatment, and the outcome of cancer. The most common variations in the genome are single-nucleotide polymorphisms (SNPs).
This study aimed to find the correlation between IL1β−511 cytokine gene and XRCC1 gene polymorphisms and the severity of liver disease and their use as a predictor to the presence of HCC. 100 subject were included in this study and they were divided in four groups. Group 1 include twenty patients were diagnosed as HCC on top of chronic HCV, group 2 include twenty patients were diagnosed as chronic Hepatitis C virus infection (CHC), group 3 include 10 patients with hepatocellular carcinoma (HCC). Group 4 include 50 healthy volunteers with no liver disease.