Hepatitis C and Liver Cancer

January 22, 2011

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Hepatitis C virus (HCV) infection is also associated with the development of

liver cancer. In fact, in Japan, hepatitis C virus is present in up to 75% of

cases of liver cancer. As with hepatitis B virus, the majority of hepatitis C

virus patients with liver cancer have associated cirrhosis (liver scarring). In

several retrospective-prospective studies (looking backward and forward in time)

of the natural history of hepatitis C, the average time to develop liver cancer

after exposure to hepatitis C virus was about 28 years. The liver cancer

occurred about 8 to 10 years after the development of cirrhosis in these

patients with hepatitis C. Several prospective European studies report that the

annual incidence (occurrence over time) of liver cancer in cirrhotic hepatitis C

virus patients ranges from 1.4 to 2.5% per year.

In hepatitis C virus patients, the risk factors for developing liver cancer

include the presence of cirrhosis, older age, male gender, elevated baseline

alpha-fetoprotein level (a blood tumor marker), alcohol use, and co-infection

with hepatitis B virus. Some earlier studies suggested that hepatitis C virus

genotype 1b (a common genotype in the U.S.) may be a risk factor, but more

recent studies do not support this finding.

The way in which hepatitis C virus causes liver cancer is not well understood.

Unlike hepatitis B virus, the genetic material of hepatitis C virus is not

inserted directly into the genetic material of the liver cells. It is known,

however, that cirrhosis from any cause is a risk factor for the development of

liver cancer. It has been argued, therefore, that hepatitis C virus, which

causes cirrhosis of the liver, is an indirect cause of liver cancer.

On the other hand, there are some chronic hepatitis C virus infected individuals

who have liver cancer without cirrhosis. So, it has been suggested that the core

(central) protein of hepatitis C virus is the culprit in the development of

liver cancer. The core protein itself (a part of the hepatitis C virus) is

thought to impede the natural process of cell death or interfere with the

function of a normal tumor suppressor (inhibitor) gene (the p53 gene). The

result of these actions is that the liver cells go on living and reproducing

without the normal restraints, which is what happens in cancer.

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