The focus of the study is to identify viral factors and host immune responses that differentiate HBV-related HCC patients from HBV patients who have not progressed to HCC. To that end, the investigators will compare gene expression levels between HCC patients and non-HCC patients categorized into high and low risk profiles. The investigators will perform ANOVA to compare three groups (HCC, high risk, low risk). Multiple comparison corrections will be performed using Benjamini and Hochberg False Discovery Rate (FDR) with a 90% confidence that the discovery lists will contain no more than 5% false positives (FDR<0.05) (PMID: 12584122, 11682119). A p-value <0.05 is considered statistically significant using this multiple comparison correction approach. Post-hoc Student-Newman-Keuls or Tukey tests will be used following ANOVA for comparisons of HCC patients with high risk and low risk. If data are not normally distributed when log-transformed, then Kruskall-Wallis tests will be used. ANCOVA will be used to adjust for the effects of covariates, such as age, gender, and HBV genotype (B or C). Further, the investigators often use an additional 2-fold change criterion for significance because the investigators consider a fold change of this magnitude to be biologically significant. Hierarchical clustering analyses and principal component analyses will be used to visualize how well the genes separate the groups, or to discover new subgroups. For the analysis of SNVs, the exact binomial test will be performed and p-values will be adjusted by the Benjamini-Hochberg correction.

NCT03300414

Conditions

1. Hepatocellular Carcinoma
2. Hepatitis B, Chronic

Interventions

1. Other: One time blood draw

MeSH:Hepatitis A Hepatitis B Hepatitis B, Chronic Carcinoma, Hepatocellular Liver N Liver Neoplasms Hepatitis

HPO:Hepatitis Hepatocellular carcinoma Neoplasm of the liver

Carcinogenesis 2008) Viral mutants including the A1762T/G1764A basal core promoter mutations and Pre-S region deletions are also associated with poor HCC outcomes and may be the result of selection by host immune responses and activation of endogenous cytidine deaminase by pro-inflammatory cytokines (e.g. --- G1764A ---