TY - JOUR
T1 - Large liver cell dysplasia in hepatitis B virus X transgenic mouse liver and human chronic hepatitis B virus-infected liver
AU - Koo, Ja Seung
AU - Seong, Je Kyung
AU - Park, Chanil
AU - Yu, Dae Yul
AU - Oh, Bong Kyeong
AU - Oh, Seung Hyun
AU - Park, Young Nyun
PY - 2005
Y1 - 2005
N2 - Objectives: Large liver cell dysplasia (LCD) is frequently associated with hepatitis B virus (HBV), but it remains uncertain whether it is reactive, senescent or preneoplastic. Methods: The HBX transgenic mice and normal control mice were sacrificed at 1, 3, 5, 7, 9, 11, 13 and 15 months after birth. Twenty-three cases of human B viral chronic hepatitis/cirrhosis with prominent LCD were selected. The immunohistochemical stain of proliferating cell nuclear antigen (PCNA), transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and senescence-associated β-galactosidase (SA-β-Gal) were evaluated. Results: In HBX transgenic mice, LCD was developed since 3 months and formed small nodules of hepatocellular adenoma, which progressed to hepatocellular carcinoma. The hepatocytes with LCD in HBX transgenic mice showed significantly higher PCNA-labeling index (LI) and lower TUNEL-LI than normal hepatocytes of control mice (p < 0.05). In the majority of human B viral chronic hepatitis/cirrhosis, the hepatocytes with LCD revealed higher PCNA-LI and lower TUNEL-LI than those without, when compared in each case using the same tissue block. SA-β-Gal staining showed no difference between hepatocytes with and without LCD. Conclusion: It is suggested that LCD, related to HBV, might not be just an innocent bystander, but closely related to hepatocarcinogenesis.
AB - Objectives: Large liver cell dysplasia (LCD) is frequently associated with hepatitis B virus (HBV), but it remains uncertain whether it is reactive, senescent or preneoplastic. Methods: The HBX transgenic mice and normal control mice were sacrificed at 1, 3, 5, 7, 9, 11, 13 and 15 months after birth. Twenty-three cases of human B viral chronic hepatitis/cirrhosis with prominent LCD were selected. The immunohistochemical stain of proliferating cell nuclear antigen (PCNA), transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and senescence-associated β-galactosidase (SA-β-Gal) were evaluated. Results: In HBX transgenic mice, LCD was developed since 3 months and formed small nodules of hepatocellular adenoma, which progressed to hepatocellular carcinoma. The hepatocytes with LCD in HBX transgenic mice showed significantly higher PCNA-labeling index (LI) and lower TUNEL-LI than normal hepatocytes of control mice (p < 0.05). In the majority of human B viral chronic hepatitis/cirrhosis, the hepatocytes with LCD revealed higher PCNA-LI and lower TUNEL-LI than those without, when compared in each case using the same tissue block. SA-β-Gal staining showed no difference between hepatocytes with and without LCD. Conclusion: It is suggested that LCD, related to HBV, might not be just an innocent bystander, but closely related to hepatocarcinogenesis.
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U2 - 10.1159/000082090
DO - 10.1159/000082090
M3 - Article
C2 - 15785085
AN - SCOPUS:17244382225
SN - 0300-5526
VL - 48
SP - 16
EP - 22
JO - Intervirology
JF - Intervirology
IS - 1
ER -
