Figure 5

Increased ALR expression in HBV-positive liver tissue. (A) ALR mRNA expression in liver tissue samples from patients with positive HCV (n = 10) or HBV (n = 10) infection was analyzed by quantitative RT-PCR analysis. 18S ribosomal RNA expression was measured for normalization, *P < 0.05. (B) Sections of liver tissue samples from patients with HCC and nontumorous adjacent liver tissue were analyzed for ALR immunoreactivity. Etiology of hepatocellular carcinoma (HCC) samples: without (w/o) HBV infection and no alcohol n = 12, alcohol n = 14, HBV infection n = 7; nontumorous liver tissue adjacent to HCC: without (w/o) HBV infection and no alcohol n = 5, alcohol n = 4, HBV infection n = 8. Intensity of anti-ALR staining was categorized from 0 to 3 (values are declared as mean ± SEM). *P < 0.05 HBV differs from w/o HBV, alc. (C) ALR protein immunoreactivity in nontumorous liver tissue sections adjacent to HCC as described in (B), (i) without (w/o) HBV infection and no alcohol, (ii) alcohol intoxication and iii) HBV infection. ALR expression was detected in the majority of hepatocytes (i–iii) and in cholangiocytes (ii), but was negative in non-parenchymal liver cells (48). (i–iii, magnification 250×).