Evidence map›Paper›PMID 41892825›Full record

ReviewMedical sciences (Basel, Switzerland)2026

Translating Fibrosis to Malignancy: Biomarkers and Therapeutic Opportunities in Liver Fibrosis and Hepatocellular Carcinoma.

Daniel Neureiter, Tobias Kiesslich, Matthias Ocker

Abstract readReview
In one paragraph

Review in Medical sciences (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

3 authors.

Daniel NeureiterInstitute of Pathology, Paracelsus Medical University, University Hospital Salzburg (SALK), 5020 Salzburg, Austria.ORCID 0000-0001-9155-5762
Tobias KiesslichCenter of Physiology, Pathophysiology and Biophysics, Institute of Physiology and Pathophysiology Salzburg, Paracelsus Medical University, 5020 Salzburg, Austria.ORCID 0000-0001-5403-9478
Matthias OckerMedical Department, Division of Hematology, Oncology and Cancer Immunology, Campus Charité Mitte, Charité University Medicine Berlin, 10117 Berlin, Germany.ORCID 0000-0001-8263-6288

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesHepatocellular carcinoma (HCC) commonly arises from chronic liver diseases that show progressing fibrosis and cirrhosis. The molecular mechanisms driving the transition from advanced fibrosis to overt malignancy remain poorly defined, representing a key knowledge gap in current hepatology research. This review delineates shared pathways like TGFβ/SMAD, WNT/β-catenin, Hedgehog, NOTCH, Hippo/YAP-TAZ and MAPK, linking fibrosis to HCC and opening avenues for dual antifibrotic/antitumor therapies. RESULTS AND

conclusionsSo far, validated biomarker tools for fibrosis, like FIB-4, Enhanced Liver Fibrosis (ELF) and combined direct/indirect markers of liver damage and tissue remodeling, are used for fibrosis staging, while HCC detection leverages serum parameters like α-fetoprotein (AFP) or, more recently, multi-omics approaches (miRNA, cfDNA, metabolomics). Understanding the interconnection of these pathways can lead to novel targeted therapies (e.g., TGFβ inhibitors) that may show dual antifibrotic and antitumor activity in future studies.

Indexed as

Biomarkers, TumorCarcinoma, HepatocellularLiver CirrhosisLiver NeoplasmsAnimalsBiomarkersHumansSignal TransductionBiomarkersBiomarkers, Tumorbiomarkercirrhosisfibrosishepatocellular carcinomaliver cancertargeted therapies

Identifiers

PMID41892825
PMCPMC13027833

What OpenQuestion holds

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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 OpenQuestion graph.