Background: To investigate the dynamic expression of IGF-II and IGFBP-3 and its alteration of bcl-2 in HCC. Methods: HCC models were induced with 2-FAA on male SD rats. Morphological changes of livers were observed and the dynamic changes of liver or serum IGF-II, IGFBP-3, and bcl-2 were quantitatively analyzed by ELISA. The expression and distribution of liver IGF-II were observed by immunohistochemistry. Result: Hepatocytes from granule-like degeneration to a typical hyperplasia to HCC and the progressing increasing of the levels of hepatic IGF-II after rats induced by 2-FAA. The levels of IGF-II in hepatoma and sera were significantly higher than any of other groups. The positive relationship of IGF-II was found between liver and sera (P<0.01). The IGFBP-3 levels in hepatoma were significantly lower than that in other groups (P<0.01) and the progressing increasing of the levels of hepatic bcl-2 expression during the course. The levels of bcl-2 in hepatoma tissues were significantly higher than those in normal and degeneration ones. The immunohistochemistry evidences indicated the positive expression and hepatocyte distribution of bcl-2 in rat hepatoma. Conclusion: Hepatic IGF-II, IGFBP-3 and bcl-2 may participate in hepatocyte canceration and accelerate the occurrence and development of HCC. The expression of IGF-II and IGFBP-3 could be useful molecular markers for early diagnosis and prognosis of HCC. Background: This study was done to assess the etiological role of hepatitis B virus (HBV), hepatitis C virus (HCV) and aflatoxin B1(AFB1) in development of hepatocellular carcinoma (HCC) in Bangladesh. It was also investigated whether alpha-feto protein (AFP) and protein induced by vitamin K absence or antagonist II (PIVKA-II) has any diagnostic advantage over each other Methods: Fifty five histologically proven HCC patients were tested for serological markers of hepatitis B and hepatitis C, and AFB1-DNA adduct. During the diagnosis, they were also investigated for liver function tests, AFP PIVKA-II. Results: Out of fifty five HCC patients, 41(74.5%) were found positive for serological markers of HBV, 21(38%) for HCV and 15(27%) for both. Eight cases (14.5%) were negative for the markers of HBV and HCV. However, none had AFB1-DNA adduct above normal range. Both PIVKA-II and AFP is strong marker for HCC with satisfactory level of sensitivity and specificity; but PIVKA-II is more sensitive (92.7%) and AFP is more specific (96%). Conclusions: HBV and HCV is the major etiological agent responsible for the development of HCC in Bangladesh. Background: To investigate the influences on the malignant transformation of hepatocytes through the intervention of NF-B activation pathway. Method: HCC models were induced with 2-FAA on SD rats, thalidomide was administered intragastrically and rats were sacrificed fortnightly interval to the twelfth week. Morphological changes were observed by HE staining. NF-B expressions were detected by IHC. The relationship between NF-B expression and pathological characteristics in HCC and non-HCC were analyzed. Results: Rat hepatocytes showed vacuole-like denaturations at the early stages, then dysplastic nodules appeared at middle stage, and finally progressed to tubercles of cancerous nest, all of which were highly differentiated HCC. Thalidomine can repress the morphologic change of liver cells. There were only punctiform denaturations at the early and middle stage; Nodosity hyperplasy and minority atypical hyperplasia were found at the finally stage. The IHC results demonstrated that NF-B level was significantly higher than those in normal ones, and the NF-B level of livers in HCC was higher than those in thalidomide group. An increasing tendency of NF-B was found from normal to HCC. NF-B in HCC were significantly higher than those in NC. The NF-B levels with thalidomide intervence raised first and decreased later. NF-B expressions in HCC were higher than that in their non-cancerous tissues. No positive relationship presented between NF-B expression and histological differentiation grade or the number of tumor, and size of tumor. Conclusion: Decrease NF-B expression can inhibit HCC development and NF-B is expected to be a new molecular target of HCC therapy. Method: The cellular distributions of VEGF expression in HCC tissues were investigated by immunohistochemistry. The levels of total RNA and VEGF were quantitatively detected in HCC, their paracancerous, and distal cancerous tissues, respectively. Simultaneitily, serum VEGF were analyzed in patients with chronic liver diseases for clinical values. Results: The positive expression showed palm-yellow or palm-brown granules and distributed in hepatocyte plasma of HCCs. The incidence of VEGF was 63.9% in HCC tissues, 78.3% in non-encapsulated HCCs, and 90.9% in HCCs with extrahepatic metastasis, respectively. No significant difference was found between hepatic VEGF and HCC diameter or differentiation degree. The specific concentration (pg/mg liver) of VEGF expression was significantly higher (P<0.01) in HCC than their paracancerous or distal cancerous tissues, respectively. The circulating VEGF was abnormally elevated in HCC. If the cut off values was more than 280 pg/mL, the incidence of serum VEGF was 88.4% in HCC, 14.3% in chronic hepatitis, and 10% in liver cirrhosis, respectively. The combined VEGF and AFP can increase positive rate up to 94.2% for HCC. Conclusion: The VEGF overexpression is a useful marker for vascular invasion and metastasis of liver tumors. Background: Hepatocellular carcinoma (HCC) represents a major health problem world wide. It accounts for 90% of all primary liver cancers and is the fifth most common malignancy (1). Objectives: Evaluation of radiofrequency thermal ablation versus transarterial hepatic chemoembolization with the effect of Viscum (Fraxini 2) on tumour recurrence. Methods: 60 patients with HCC were enrolled in the study. Group 1 include 30 patients and were treated with radiofrequency thermal ablation (15 patients of them received viscum 2 by subcutaneous route for 2 years). Group 11 included 30 patients with HCC and were treated by TACE (15 patients of them received viscum 2 subcutaneously for 2 years). Results: Group 1 patients showed total ablation in 70% with persistant inactivity during 2 years follow up. Group 11 did not show significant difference from Group 1 as regards relapse rate nor the performance status. Complications as nausea, vomiting, fever, jaundice, and elevation of transaminases were significantly more encountered with TACE. Viscum 2 did not significantly arrest tumour recurrence. Conclusion: Non surgical patients with HCC can achieve curative treatment with radiofrequency with minmal side effects. TACE is a palliative treatment option for large HCC.