ReviewGenes2018
Hepatitis B Virus-Associated Hepatocellular Carcinoma and Hepatic Cancer Stem Cells.
Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Exploring the anticancer potential of nitrated N-substituted-4-hydroxy-2-quinolone-3-carboxamides: synthesis, biological assessment, and computational analysis.BMC chemistry · 2025Article
- Galectins and Liver Diseases.International journal of molecular sciences · 2025Review
- Targeting Hepatic Cancer Stem Cells (CSCs) and Related Drug Resistance by Small Interfering RNA (siRNA).Cell biochemistry and biophysics · 2024Review
- The role of oncolytic virotherapy and viral oncogenes in the cancer stem cells: a review of virus in cancer stem cells.Cancer cell international · 2023Review
- Galectin-9 in cancer therapy: from immune checkpoint ligand to promising therapeutic target.Frontiers in cell and developmental biology · 2023Review
- Review
- Viral hepatitis and hepatocellular carcinoma: From molecular pathways to the role of clinical surveillance and antiviral treatment.World journal of gastroenterology · 2022Review
- Article
- Article
- Galectin-9 expression predicts poor prognosis in hepatitis B virus-associated hepatocellular carcinoma.Aging · 2022Article
- Progress of HOTAIR-microRNA in hepatocellular carcinoma.Hereditary cancer in clinical practice · 2022Review
- Hepatitis B Virus Pregenomic RNA Reflecting Viral Replication in Distal Non-tumor Tissues as a Determinant of the Stemness and Recurrence of Hepatocellular Carcinoma.Frontiers in microbiology · 2022Article
- Exosomal miR-4800-3p Aggravates the Progression of Hepatocellular CarcinomaFrontiers in oncology · 2022Article
- Review
- Non-cirrhotic hepatocellular carcinoma in chronic viral hepatitis: Current insights and advancements.World journal of gastroenterology · 2021Review
- Review
- The Prevalence of Hepatitis B Virus Markers among Students of Shiraz University of Medical Sciences.Advanced biomedical research · 2021Article
- Immunotherapy for targeting cancer stem cells in hepatocellular carcinoma.Theranostics · 2021Review
- Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma.World journal of gastroenterology · 2020Review
- Hepatitis B Virus Pre-S Mutants as Biomarkers and Targets for the Development and Recurrence of Hepatocellular Carcinoma.Viruses · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic Hepatitis B Virus (HBV) infection is linked to hepatocellular carcinoma (HCC) pathogenesis. Despite the availability of a HBV vaccine, current treatments for HCC are inadequate. Globally, 257 million people are chronic HBV carriers, and children born from HBV-infected mothers become chronic carriers, destined to develop liver cancer. Thus, new therapeutic approaches are needed to target essential pathways involved in HCC pathogenesis. Accumulating evidence supports existence of hepatic cancer stem cells (hCSCs), which contribute to chemotherapy resistance and cancer recurrence after treatment or surgery. Understanding how hCSCs form will enable development of therapeutic strategies to prevent their formation. Recent studies have identified an epigenetic mechanism involving the downregulation of the chromatin modifying Polycomb Repressive Complex 2 (PRC2) during HBV infection, which results in re-expression of hCSC marker genes in infected hepatocytes and HBV-associated liver tumors. However, the genesis of hCSCs requires, in addition to the expression of hCSC markers cellular changes, rewiring of metabolism, cell survival, escape from programmed cell death, and immune evasion. How these changes occur in chronically HBV-infected hepatocytes is not yet understood. In this review, we will present the basics about HBV infection and hepatocarcinogenesis. Next, we will discuss studies describing the mutational landscape of liver cancers and how epigenetic mechanisms likely orchestrate cellular reprograming of hepatocytes to enable formation of hCSCs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.