Lack of colocalization of HBxAg and insulin like growth factor II in the livers of patients with chronic hepatitis B, cirrhosis and hepatocellular carcinoma.

To evaluate the possibility that HBxAg is related to an enhanced expression of IGF-II, immunohistochemical staining was performed for distribution and colocalization of HBxAg and IGF-II in liver tissues from 40 chronic active hepatitis (CAH-B), 51 cirrhosis and 46 hepatocellular carcinoma (HCC) patients using polyclonal rabbit anti HBxAg raised against full length-recombinant HBxAg and monoclonal mouse anti IGF-II. HBxAg in CAH-B, cirrhosis and HCC tissues was detected in 95%, 39% and 17%, whereas IGF-II in the same tissues was seen in 0%, 92% and 100%, respectively. There was a gradual decrease in the prevalence of HBxAg expression in cirrhosis and HCC, as compared to CAH-B tissues. All of the cirrhosis and HCC samples with positive staining for HBxAg expressed IGF-II. However, 55% of cirrhosis and 100% of HCC samples without HBxAg staining also expressed IGF-II. Moreover, colocalization at neighboring sections, even in both HBxAg and IGF-II positive samples, was not regularly observed. It is concluded that HBxAg expression in CAH-B may play a role in the pathogenesis of CAH-B. Although HBxAg may be related to the expression of IGF-II in some cirrhotic and HCC tissues, IGF-II expression in a large majority of these cases may be related to other factor(s) than HBxAg.