Evidence map›Paper›PMID 38003240›Full record

ReviewInternational journal of molecular sciences2023

HCV and HCC Tango-Deciphering the Intricate Dance of Disease: A Review Article.

Ivana Milosevic, Nevena Todorovic, Ana Filipovic, Jelena Simic, Marko Markovic, Olja Stevanovic, Jovan Malinic, Natasa Katanic, Nikola Mitrovic, Natasa Nikolic

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Ubiquitination in hepatocellular carcinoma immunity.Journal of translational medicine · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Ivana MilosevicFaculty of Medicine, Department for Infectious Diseases, University of Belgrade, 11000 Belgrade, Serbia.
Nevena TodorovicUniversity Clinic for Infectious and Tropical Diseases, University Clinical Center of Serbia, Bulevar Oslobodjenja 16, 11000 Belgrade, Serbia.
Ana FilipovicUniversity Clinic for Infectious and Tropical Diseases, University Clinical Center of Serbia, Bulevar Oslobodjenja 16, 11000 Belgrade, Serbia.
Jelena SimicUniversity Clinic for Infectious and Tropical Diseases, University Clinical Center of Serbia, Bulevar Oslobodjenja 16, 11000 Belgrade, Serbia.
Marko MarkovicFaculty of Medicine, Department for Infectious Diseases, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0009-0002-3574-3341
Olja StevanovicFaculty of Medicine, Department for Infectious Diseases, University of Belgrade, 11000 Belgrade, Serbia.
Jovan MalinicFaculty of Medicine, Department for Infectious Diseases, University of Belgrade, 11000 Belgrade, Serbia.
Natasa KatanicUniversity Clinic for Infectious and Tropical Diseases, University Clinical Center of Serbia, Bulevar Oslobodjenja 16, 11000 Belgrade, Serbia.
Nikola MitrovicFaculty of Medicine, Department for Infectious Diseases, University of Belgrade, 11000 Belgrade, Serbia.
Natasa NikolicFaculty of Medicine, Department for Infectious Diseases, University of Belgrade, 11000 Belgrade, Serbia.
University of Belgrade · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a major cause of hepatocellular carcinoma (HCC) accounting for around one-third of all HCC cases. Prolonged inflammation in chronic hepatitis C (CHC), maintained through a variety of pro- and anti-inflammatory mediators, is one of the aspects of carcinogenesis, followed by mitochondrial dysfunction and oxidative stress. Immune response dysfunction including the innate and adaptive immunity also plays a role in the development, as well as in the recurrence of HCC after treatment. Some of the tumor suppressor genes inhibited by the HCV proteins are p53, p73, and retinoblastoma 1. Mutations in the telomerase reverse transcriptase promoter and the oncogene catenin beta 1 are two more important carcinogenic signaling pathways in HCC associated with HCV. Furthermore, in HCV-related HCC, numerous tumor suppressor and seven oncogenic genes are dysregulated by epigenetic changes. Epigenetic regulation of gene expression is considered as a lasting "epigenetic memory", suggesting that HCV-induced changes persist and are associated with liver carcinogenesis even after cure. Epigenetic changes and immune response dysfunction are recognized targets for potential therapy of HCC.

Indexed as

Carcinoma, HepatocellularHepatitis CLiver NeoplasmsCarcinogenesisEpigenesis, GeneticHepacivirusHumansepigenetic changeshepatitis C virushepatocellular carcinomaimmune dysregulationoncogenesis

Identifiers

PMID38003240
PMCPMC10671156
OpenAlexW4388446775

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.