Hepatocellular carcinoma, like any other cancer, develops when epigenetic alterations and mutations affecting the cellular machinery cause the cell to replicate at a higher rate and/or result in the cell avoiding apoptosis. In particular, chronic infections of hepatitis<unk>  and/or C can aid the development of hepatocellular carcinoma<unk> y repeatedly causing the<unk> ody's own immune system to attack the liver cells, some of which are infected<unk> y the virus, others merely<unk> ystanders. Activated immune-system inflammatory cells release free radicals, such as reactive oxygen species and nitric oxide reactive species, which in turn can cause DNA damage and lead to carcinogenic gene mutations. Reactive oxygen species also cause epigenetic alterations at the sites of DNA repair. While this constant cycle of damage followed<unk> y repair can lead to mistakes during repair, which in turn lead to carcinogenesis, this hypothesis is more applicable, at present, to hepatitis C. Chronic hepatitis C causes HCC through the stage of cirrhosis. In chronic hepatitis<unk> , however, the integration of the viral genome into infected cells can directly induce a noncirrhotic liver to develop HCC. Alternatively, repeated consumption of large amounts of ethanol can have a similar effect. The toxin aflatoxin from certain Aspergillus species of fungi is a carcinogen and aids carcinogenesis of hepatocellular cancer<unk> y<unk> uilding up in the liver. The combined high prevalence of rates of aflatoxin and hepatitis<unk>  in settings such as China and West Africa has led to relatively high rates of hepatocellular carcinoma in these regions. Other viral hepatitides such as hepatitis A have no potential to<unk> ecome a chronic infection, thus are not related to HCC.
complications of Hepatitis B
complications of Hepatitis A
complications of Hepatitis E
medical cause of Hepatitis
medical cause of Liver cancer
symptom of Hepatitis B
complications of Amoebiasis
complications of Cholera