AIM:To investigate the serum level and expression of insulingrowth factor Ⅱ(IGF-Ⅱ)in liver tissues of rats with earlyexperimental hepatocellular carcinomas(HCC)and itssignificance in early diagnosis.METHODS:Early experimental hepatocellular carcinomaswere induced by diethylnitrosamine(DENA)in 180 male SDrats.Another 20 male SD rats served as control.The IGF-Ⅱserum level was measured by ELISA.Immunohistochemistryand electron microscopic immunohistochemistry were usedto observe the expression of IGF-Ⅱ in normal and tumorliver tissues and its ultrastructural location in malignanthepatocytes.The expressions of IGF-Ⅱ in human hepatomacell lines HepG2,SMMC7721 and human embryonic livercell line L-02 were measured by immunocytochemistry.IGF-II mRNA level was studied by in situ hybridization.RESULTS:IGF-Ⅱ was expressed in the cytoplasm of bothsinusoidal cells in paracancerous cirrhotic liver tissue andmalignant hepatocytes in early experimental HCC tissues.Gold particles were seen on the rough endoplasmic reticulumand the mitochondrion in malignant hepatocytes.IGF-Ⅱ wasexpressed in the human hepatoma cell lines.The mRNAlevel of IGF-Ⅱ was higher in rat liver tumor tissue than innormal rat liver tissue.The serum IGF-Ⅱ level of the earlyexperimental HCC group was 34.67±10.53 ng.ml~(-1)and thatof the control group was 11.75±5.84 ng.ml~(-1).The rank sumtest was used for statistical analysis.There was a significantdifference between the two groups(P<0.01).CONCLUSION:During the induction of early experimentalHCC by DENA,IGF-Ⅱ may promote hepatocytic proliferationvia a paracrine mechanism in the pre-cancerous stage.Whenhepatocytes are transformed into malignant cells,they maysecrete IGF-Ⅱ and promote malignant cell proliferation byan autocrine mechanism.IGF-Ⅱ may be a possible biologicalmarker in the early diagnosis of HCC. AIM: To investigate the serum level and expression of insulingrowth factor II (IGF-II) in liver tissues of rats with early experimental hepatocellular carcinomas (HCC) and itssignificance in early diagnosis. METHODS: Early experimental hepatocellular carcinomas induced by diethylnitrosamine (DENA) in 180 male SDrats. Another 20 male SD rats served as control. IGF-II serum level was measured by ELISA. Immunohistochemistry and electron microscopic immunohistochemistry were used to observe the expression of IGF-II in normal and tumorliver tissues and its ultrastructural location in malignant hepatic cells. The expressions of IGF-II was expressed in the cytoplasm of both hepatoma cell lines HepG2, SMMC7721 and human embryonic liver cell line L-02 were measured by immunocytochemistry. IGF-II mRNA level was studied by in situ hybridization. cirrhotic liver tissue andmalignant hepatocytes in early experimental HCC tissues. Gold particles were seen on the rough endoplasmic reticulumand the mitochondrion in malignant hepatocytes. IGF-II wasexpressed in the human hepatoma cell lines. The mRNA level of IGF-II was higher in rat liver tumor tissue than innormal rat liver tissue. serum IGF-II level of the early experimental The rank sum test was used for statistical analysis. There was a significant difference between the two groups (HCC group was 34.67 ± 10.53 ng.ml ~ (-1) and that of the control group was 11.75 ± 5.84 ng.ml ~ (-1) P <0.01). CONCLUSION: During the induction of early experimental HCC by DENA, IGF-II may promote hepatocytic proliferationvia a paracrine mechanism in the pre-cancerous stage. Hepatocytes are transformed into malignant cells, they maysecrete IGF-II and promote malignant cell proliferation byan autocrine mechanism. IGF-II may be a possible biological marker in the early diagnosis of HCC.