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Background: p63 helps regulate differentiation and proliferation in epithelial progenitor cells. Its expression is often higher in malignant tissue compared with normal tissue, and poorly differentiated carcinomas often show a larger number of p63-positive cells than well-differentiated tumors. The aim of the present study was to investigate the immunohistochemical expression of p63 in human cholangiocarcinomas (CC) and hepatocellular carcinomas (HCC)., Methods: Sixteen cases of CC and 37 cases of HCC were selected for the present study. Paraffin-embedded sections were submitted to immunohistochemical double-staining to identify p63 and cytokeratin 19., Results: p63 was diffusely expressed in 100% of CC, while it was negative in all HCC. In addition, cytokeratin 19, a marker for hepatic progenitor cells, was colocalized in all p63-positive cells., Conclusions: The nuclear immunostaining for p63 in all CC cases indicates that the p63 protein can act to promote neoplastic growth in bile duct epithelium, but it is not important for hepatocellular carcinogenesis. Co-localization of p63 and cytokeratin 19 in CC cells suggests that CC may be derived from undifferentiated progenitor cells (hepatic oval cells). Furthermore, p63 can be useful in the differential diagnosis between CC and HCC in biopsy samples.

Background and Aims: Iron deposits in the liver and abnormalities in serum iron biochemistry are frequently observed in patients with chronic liver diseases, but data for patients with hepatitis B virus (HBV) infection are scarce. Moreover, the role of HFE mutations in iron deposits in this condition remains unknown. The aim of the present study was to determine the prevalence of serum iron biochemical abnormalities and iron deposits in the liver of chronic HBV patients, and to evaluate the consequences for the activity and severity of liver disease. Additionally, we studied the role of HFE gene mutations in iron deposits., Methods: Eighty-one male non-cirrhotic HBV patients were studied. Serum iron biochemistry, liver enzymes and C282Y/H63D mutations were investigated. Liver biopsies were scored for necroinflammatory activity (histological activity index [HAI]), fibrosis and iron deposits., Results: Elevated transferrin saturation (TS) was found in 27.1% of patients and liver iron deposits in 48.7%; these deposits were mild in 68.4% and moderate in 31.6%. Patients with liver iron deposits exhibited significantly higher scores for HAI and fibrosis than those without iron deposits. HFE mutations were identified in 23.4% of patients (14 H63D heterozygotes, four H63D homozygotes, one compound mutation). No difference in the prevalence of C282Y and H63D mutations was observed between HBV patients (1.2% and 23.4%, respectively) and the general population (4.1% and 27.8%, respectively). No association was detected between HFE mutations and elevated TS or liver iron deposits., Conclusions: Elevated TS and liver iron deposits were frequent in non-cirrhotic HBV patients. Iron deposits were mainly mild and associated with higher activity and severity of liver disease, but not with HFE mutations.

Background and Aim: To determine the relationship between hepatic stellate cell (HSC) populations and severity of liver disease and liver iron deposits in patients with chronic hepatitis C virus (HCV). We also studied the relationship between iron cellular distribution and HSC population and the role of HFE mutations in the determination of iron deposits., Methods: Forty-nine chronic HCV patients with varying degrees of liver damage and liver iron deposits were studied. A liver biopsy was scored for histology activity index (HAI), fibrosis and iron deposits. The number of HSC in the liver was evaluated by an immunohistochemical double-staining method to identify glial fibrillary acid protein (GFAP) and smooth muscle alpha-actin (alpha-SMA)., Results: The HSC population was significantly higher in HCV patients than in normal controls and was predominant in zones 1 and 3. Liver iron deposits were observed in 49% of patients and were mild/moderate in most cases. We found a significantly higher number of GFAP and alpha-SMA positive cells in patients with liver iron deposits compared with those without iron deposits, and a positive correlation between liver iron scores and number (%) of GFAP and alpha-SMA positive cells. We observed a significantly higher number of GFAP and alpha-SMA positive cells in moderate/severe hepatitis than in minimal/mild hepatitis, and a positive correlation between GFAP and alpha-SMA positive cells and HAI and fibrosis scores., Conclusions: Liver iron deposits in chronic HCV are common and are associated with activation of HSC. Thus, even mild iron deposits might stimulate HSC and contribute to liver damage.