ReviewWorld journal of hepatology2015
Hepatitis D and hepatocellular carcinoma.
Review in World journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 63 citations in OpenAlex.
- Metabolites involvement in the growth and spread of liver cancer.Liver research (Beijing, China) · 2025Review
- [Hepatocellular carcinoma (HCC)].Medecine tropicale et sante internationale · 2024Review
- Seroprevalence and molecular characterization of viral hepatitis and HIV co-infection in the Central African Republic.PloS one · 2024Article
- Hepatitis D Virus and HBsAg Dynamics in the era of new Antiviral Treatments.Current gastroenterology reports · 2023Review
- An Insight Into the Factors Affecting the Prevalence and Natural History of Hepatitis D.Cureus · 2023Review
- Molecular and Clinical Features of Hepatocellular Carcinoma in Patients with HBV-HDV Infection.Journal of hepatocellular carcinoma · 2023Review
- Review
- Viral hepatitis and hepatocellular carcinoma: From molecular pathways to the role of clinical surveillance and antiviral treatment.World journal of gastroenterology · 2022Review
- Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?International journal of molecular sciences · 2022Review
- Role of Histone Post-Translational Modifications in Inflammatory Diseases.Frontiers in immunology · 2022Review
- Present and future management of viral hepatitis.World journal of gastroenterology · 2021Review
- Hepatitis B/D-Related Hepatocellular Carcinoma. A Clinical Literature Review.Journal of gastrointestinal cancer · 2021Review
- Hepatitis D Virus and Hepatocellular Carcinoma.Viruses · 2021Review
- Hepatitis D virus and liver transplantation: Indications and outcomes.World journal of hepatology · 2021Review
- HBV/HDV Co-Infection: Epidemiological and Clinical Changes, Recent Knowledge and Future Challenges.Life (Basel, Switzerland) · 2021Review
- Effect of HBV-HDV co-infection on HBV-HCC co-recurrence in patients undergoing living donor liver transplantation.Hepatology international · 2020Article
- HBV/HDV Coinfection: A Challenge for Therapeutics.Clinics in liver disease · 2019Review
- Hepatitis D infection: from initial discovery to current investigational therapies.Gastroenterology report · 2019Article
- Hepatitis D virus infection, cirrhosis and hepatocellular carcinoma in The Gambia.Journal of viral hepatitis · 2019Article
- Pathogenesis of and New Therapies for Hepatitis D.Gastroenterology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis D virus (HDV) is a defective circular shape single stranded HDV RNA virus with two types of viral proteins, small and large hepatitis D antigens, surrounded by hepatitis B surface antigen. Superinfection with HDV in chronic hepatitis B is associated with a more threatening form of liver disease leading to rapid progression to cirrhosis. In spite of some controversy in the epidemiological studies, HDV infection does increase the risk of hepatocellular carcinoma (HCC) compared to hepatitis B virus (HBV) monoinfection. Hepatic decompensation, rather than development of HCC, is the first usual clinical endpoint during the course of HDV infection. Oxidative stress as a result of severe necroinflammation may progress to HCC. The large hepatitis D antigen is a regulator of various cellular functions and an activator of signal transducer and activator of transcription (STAT)3 and the nuclear factor kappa B pathway. Another proposed epigenetic mechanism by which HCC may form is the aberrant silencing of tumor suppressor genes by DNA Methyltransferases. HDV antigens have also been associated with increased histone H3 acetylation of the clusterin promoter. This enhances the expression of clusterin in infected cells, increasing cell survival potential. Any contribution of HBV DNA integration with chromosomes of infected hepatocytes is not clear at this stage. The targeted inhibition of STAT3 and cyclophilin, and augmentation of peroxisome proliferator-activated receptor γ have a potential therapeutic role in HCC.
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.