English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background:  Hepatitis B virus (HBV) is a causative agent of hepatocellular carcinoma (HCC). Until now, the mechanism behind the progress of hepatitis B fibrosis to HCC remains largely unknown. This study aims to examine the candidate biomarkers and pathways involved in HBV-associated HCC.   Methods:  Gene expression profiles were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using the GEO2R tool after which functional enrichment analysis, protein-protein interaction (PPI) analysis, genetic alteration analysis, prognostic analysis, immune infiltration analysis, co-expression genes prediction, and miRNA-gene network construction, and pathway correlation analysis were performed.   Results:  22 hub genes were identified, which were all highly expressed in HCC, and overexpression of these genes was all associated with significantly worse survival in HCC patients. More significantly,  ASPM  also showed increased expression levels in non-tumor tissues with advanced liver fibrosis. With the progression of liver fibrosis and the closer tumor center of HCC, the higher expression of  ASPM  was identified.  ASPM  was considered to be the most promising biomarker because it also showed the highest genetic alteration frequency among the hub genes and the expression level of  ASPM  in HBV (+) HCC tissues was significantly higher than that in HBV (-) HCC tissues. Also, the infiltration levels of B cells, CD8 +  T cells, CD4 +  T cells, macrophages, neutrophils, and dendritic cells were all positively correlated with the expression of  ASPM .   Conclusion:  These findings may help in the development of strategies and candidate drugs for the treatment of HBV-related HCC and improve the effectiveness of personalized treatment in the future.  ASPM  was upregulated in both hepatitis B cirrhosis and HCC and could be a potential predicting biomarker.

ASPM May be Related to the Malignant Progression of Hepatitis B and is Associated With a Poor Prognosis of Hepatocellular Carcinoma