Methods: This open-label study was conducted in 5 major hospitals in China. At study entry all patients had HBV DNA levels 10 7 copies/mL, elevated ALT (1.3-10xULN) and compensated liver function. Patients received either 0.5mg ETV or 100mg LVD daily. HBV DNA measurements were taken at baseline and at Weeks 2, 4, 12 and 24 during treatment, using Roche Cobas Amplicor assay (LLOD 300 copies/mL). Results: A total of 97 patients were enrolled; 42/50 ETV patients and 40/47 LVD patients completed 24 weeks of treatment. At baseline, mean HBV DNA levels were 8.45 0.81 in ETV group and 7.67 1.76 log 10 copies/mL in LVD group (P<0.05). The mean change in HBV DNA from baseline (log10 copies/mL) was -2. 96±0 NGO's/Funding-agencies representative at APASL2009-conference need to address-this-issue. We NGO-representatives from developing-nations need exposure to research treatments used by European/American experts. Do we all failed in addressing socio-economic issues of cancer-sufferers? We need to address these socio-economic issues of affected population in resource-poor-nations. Background: A garlic derivative S-allylcysteine (SAC) has anti-cancer effect in human prostate and colon cancers. We aimed to investigate the effect of SAC and combination of chemo-drug on tumorigenesis and metastasis of liver cancer. Methods: The orthotopic liver tumor model using a metastatic liver cancer cell line MHCC97L labeled with luciferase gene was applied. SAC was given at day 7 after tumor implantation at 1mg/g/day, or 1mg/g/day combined with low dose Cisplatin for 5 weeks. Tumor growth and metastasis were monitored by Xenogen in vivo imaging system. Hepatic stellate cell (HSC) activation and tumor-associated macrophage (TAM) in the tumor tissue were detected by -SMA and ED1/ED2 staining. Tumor micro-vessel density (MVD) and apoptosis were also analyzed. In vitro functional tests including proliferation assay, cell cycle analysis and apoptosis analysis were performed. Results: Tumor growth was inhibited by SAC combined with Cisplatin treatment at different time points accompanied by lower incidence of lung metastasis compared with other groups. The observation of Xenogen IVIS was confirmed by histopathological examination. The HSC activation by -SMA staining in the liver tumors was suppressed by SAC and Cisplatin treatment accompanied with less TAM infiltration. Consistent with in vivo study, in vitro functional study also demonstrated that SAC not only induced cell cycle arrest, apoptosis, and inhibited tumor cell proliferation, but also sensitized the anti-cancer effect of Cisplatin. Conclusion: SAC treatment inhibited liver tumor growth and metastasis by inhibiting tumor cell proliferation, inducing apoptosis and sensitization of chemotherapy. Background: Anti-angiogenic therapy would be a promising approach against hepatocellular carcinoma (HCC). Although a sorafenib has survival benefits in patients at advances stages of HCC, there seem to be several serious concerns to employ this agent for chemoprevention against HCC. Branched-chain amino acid (BCAA) reportedly inhibits the incidence of HCC in patients with insulin resistance (IR). However, the possible mechanism is still obscure. The aim of the current study was to examine the effect of BCAA on hepatocarcinogenesis under the condition of IR, especially in conjunction with angiogenesis. Methods: The effect of BCAA on the development of liver enzyme-altered pre-neoplastic lesions and angiogenesis in the obese diabetic Otsuka Long-Evans Tokushima Fatty rats was examined. We also performed an in-vitro study to elucidate the possible mechanisms involved. Result: Treatment with BCAA markedly inhibited the glutathione-S-transferase placental form (GST-P)-positive pre-neoplastic lesions along with suppression of neovascularization in the liver. The hepatic expression of the vascular endothelial growth factor (VEGF), a potent angiogenic factor, was also attenuated. BCAA treatment significantly suppressed the glucose-and insulin-induced in-vitro angiogenesis in the presence of VEGF. These results indicate that BCAA exerted a chemopreventive effect under the condition of IR via suppression of VEGF-mediated angiogenesis. Conclusion: Since BCAA is widely used in the clinical practice for patients with chronic liver diseases, this agent may represent a new strategy for chemoprevention against IR-based HCC in the future. 