Hua Tang 1 , Xiao-Yan Tang 1 , Min Liu 1 , Xin Li 1 1 Tianjin Life Science Research Center, Tianjin Medical University, Tianjin 300070, China We determined how AFP modulates the proliferation of hepatoma cells. A recombinant adenovirus expressing siRNA against AFP (Adv-AFPsiRNA) was created and found that it reduced expression of AFP specifically in hepatoma cells, and markedly inhibited the proliferation of hepatoma cells in vitro. Local treatment using Adv-AFPsiRNA caused significant repression of the growth of hepatoma derived HepG2 cells in xenograft in nude mice. Knockdown of AFP resulted in an obvious delay in the G1/S transition of cell cycle, but did not affect apoptosis in HepG2 cells, as analyzed by flow cytometry and TUNEL assay. Also, differential expressions of some genes related to the cell cycle, including SKP2, Cyclin D1, Csk and EBAG9 were identified by microarray and RT-PCR in HepG2 cells and HepG2 cells with knocked down AFP. These results suggest that endogenous AFP is a critical determinant of the growth of hepatoma cells. Hematopoietic stem cell (CD 34+) therapy can improve liver function in patients with cirrhosis. These cells can be mobilized into peripheral blood using Granulocyte colony stimulating factor (GCSF). This study was undertaken to assess feasibility and safety and of GCSF induced CD 34+ cell mobilization and its impact on liver function in patients with cirrhosis. Patients with liver cirrhosis (Cryptogenic or alcoholic with 6m abstinence) with CPT > 7 and < 12, and splenic diameter < 17 cm were included. GCSF injection was given for 5 days (5mcg/kg/dose). Baseline & day-6 CD 34+ counts in peripheral blood were done by flow cytometry. Follow up was weekly for 4 weeks and then monthly. CPT was compared at baseline and 6 months. 9 Patients (median age 51 y, range 33-64 y, 8 males; etiology: 6 alcohol, 3 cryptogenic; median CPT 10, range 8-12) were included. CD 34 + cell counts at baseline and day 6 were 2(0-3) and 15 (13-41) respectively (median, range). Side effects were fever in 8, allergic reaction in 1 and increase in splenic size in 1 (excluded). In follow up, 3 patients died (1, 3 & 4m after therapy, 1 after OLT), 1 lost to follow-up. 4 patients showed improvement in 10 -7) at 6-month follow-up. GCSF treatment is safe and yields adequate CD 34+ cells in peripheral blood. In short term it results in improvement in liver function in patients with cirrhosis PE415 Molecular cloning and Transcriptional analysis of KCTD9 gene promoter B. Pi 1 , J.S. Wang 1 , M.F. Han 1 , Y.Y. Zhou 1 , X.J. Liu 1 , X.P. Luo 2 , Q. Ning 1 1 Department of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 2 Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Aim: Our previous work has shown that high expression of KCTD9, a potassium channel associated gene, correlated with the disease severity of patients with severe chronic hepatitis B(SCHB). To further understand the gene transcription and regulation, KCTD9 promoter was cloned and gene transcription was studied. Methods: A full length of isolated promoter and series of 5' truncated promoter of KCTD9 gene was subcloned into the luciferase report vector pGL2-basic to form the promoter-report constructs. The KCTD9 promoter-report construct upstream of the luciferase report gene was cotransfected with constructs expressing HBV X,C and S protein respectively or stimulated with cytokines (IL-2, IFN and TNF ) in 293 T cells to investigate KCTD9 gene regulation upon both viral factors and host cytokines. Result: A 759bp KCTD9 segment upstream of ATG translation start site was evidenced to contain potential regulative domains. An important regulation site located between -268bp and -81bp upstream of ATG translation start site. Based upon the luciferase activity assay, IL-2 was able to upregulate the transcription of KCTD9 whereas there was no effect from neither HBV viral proteins nor IFN and TNF . Conclusion: Here we first successfully cloned the full length promoter of KCTD9. IL-2 significantly enhanced the transcription of KCTD9, a gene which has been shown to be involved in T cell activation and disease severity of SCHB from our group. This work was supported by NSFC(30571643, 30672380, 30700702) 1 1 Istanbul University, Cerrahpasa Medical School, 2 Marmara University, 3 Okmeydani Teaching Hospital, 4 