[68] Recently, Hamaoka et al. showed peripheral platelet counts at the time of HCC detection were greater in females with homozygous deletion at nt −155 and C/C Pifithrin-�� mouse or C/T at nt −443 than in those showing other alleic combinations among the hepatitis patients with HCV infection, while no such difference was observed in males.[68] It is well known that the platelet counts decrease with the progression of liver fibrosis in patients

with persistent HCV infection. Thus, HCC may develop in the early stage of liver fibrosis after HCV infection in females with such a genetic background. Dong et al. demonstrated that OPN SNP at nt −443 was significantly associated with OS and time selleck to recurrence (TTR) in the patients with HCC.[69] Multivariate analysis identified allele C/C at nt −443 as a significant independent predictor of increased OS and long TTR. Tumor growth and lung metastasis were

enhanced in nude mice implanted with HepG2 cells transfected with OPN promoter-reporter constructs containing allele T at nt −443 compared with allele C. They showed oligonucleotides with allele T at nt −443 increased transcriptional activity and OPN protein level compared with allele C.[69] However, Hamaoka et al. presented that the transcriptional activity was greater in oligonucleotides with allele C at nt −443 than in those with allele T.[68] The reason for the discrepancy remains unclear. OSTEOPONTIN IS INVOLVED in hepatic inflammation and fibrogenesis in alcoholic and non-alcoholic MCE公司 steatohepatitis. OPN is also linked to progression and metastasis of HCC. OPN expressions were observed in a variety of liver cells, including Kupffer cells, hepatic macrophages, stellate cells, bile duct cells, NKT cells, hepatocytes and HCC cells. OPN is altered through cleavage, splicing or post-translational modifications and has two isoforms, sOPN and iOPN. Recently, OPN was shown to be a downstream effecter of Hedgehog pathway. Therefore, elucidation

of a multiplicity of functions of OPN depending on the structure and cellular interactions, could develop novel therapeutics and biomarkers for the liver diseases. “
“Interleukin (IL)28B polymorphisms are associated with spontaneous clearance of hepatitis C virus (HCV) infection and response to therapy. Whether IL28B genotype affects fibrosis progression or clinical outcome is unclear. Our aim was to study the relationship between IL28B genotype and both histological and clinical outcomes in patients with chronic hepatitis C (CHC). Hepatic fibrosis was scored using the Ishak (0-6) scale; progression was defined as a 2-point increase in Ishak score between biopsies. Multiple logistic and Cox regressions were used to identify variables associated with fibrosis progression.