Evidence map›Paper›PMID 41042332›Full record

ArticleVirchows Archiv : an international journal of pathology2025

Proteomic subtyping highlights tumor heterogeneity of human HCC.

Thomas Ritz, Jovan Tanevski, Jana Baues, Sven H Loosen, Tom Luedde, Ulf Neumann, Peter Boor, Peter Schirmacher, Julio Saez-Rodriguez, Thomas Longerich

Abstract read
In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2025. 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. Article
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.

Thomas Ritz *Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany. thomas-ritz@gmx.net.ORCID http://orcid.org/0009-0008-1542-3264
Jovan Tanevski *Institute for Computational Biomedicine, Heidelberg University & Heidelberg University Hospital, Faculty of Medicine, Heidelberg, Germany.
Jana BauesInstitute of Pathology, Uniklinik RWTH Aachen, Aachen, Germany.
Sven H LoosenDepartment of Gastroenterology, Hepatology and Infectious Diseases, University Hospital Dusseldorf, Düsseldorf, Germany.
Tom LueddeDepartment of Gastroenterology, Hepatology and Infectious Diseases, University Hospital Dusseldorf, Düsseldorf, Germany.
Ulf NeumannDepartment of General-, Visceral- and Transplantation Surgery, University Hospital Essen, Essen, Germany.
Peter BoorInstitute of Pathology, Uniklinik RWTH Aachen, Aachen, Germany.
Peter SchirmacherInstitute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.
Julio Saez-RodriguezInstitute for Computational Biomedicine, Heidelberg University & Heidelberg University Hospital, Faculty of Medicine, Heidelberg, Germany.
Thomas LongerichInstitute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, 69120, Heidelberg, Germany.

Funding

Deutsche Forschungsgemeinschaft SFB/TR209
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) has a poor prognosis. While molecular profiling has identified subclasses with potentially druggable pathways, implementation in routine diagnostics remains challenging. Although immunohistology may aid HCC classification, multiplexed protein-based approaches have not yet been established. Proteomic heterogeneity in HCC tissue also remains poorly understood. Tissue microarrays from 58 HCC patients were analyzed using a multispectral imaging platform, enabling the detection of multiple protein biomarkers on a single tissue slide. A machine learning-based algorithm facilitated single-cell expression analysis, clustering, and spatial distribution assessment. A 4-plex immunofluorescence marker panel was designed and applied to interrogate altered signaling pathways in HCC. Unsupervised analysis revealed four factors corresponding to three HCC clusters defined by the overexpression patterns of p-S6/CRP (Cluster A), glutamine synthetase (Cluster B), and EpCam (Cluster C). Single-cell resolution uncovered substantial intratumoral heterogeneity. Only one third of HCCs showed a ≥ 0.95 purity of tumor cells in the predominant cluster. Clinically, Cluster C was associated with reduced median overall survival, while the other clinico-pathological features were not significantly different between the clusters. A protein-based subclassification of human HCC was established, characterized by three distinct subclasses (inflammation, beta-catenin/WNT signaling, progenitor-like) that align with known molecular categories. Cases with dominant progenitor features tended to have a shorter survival probability. The intratumoral heterogeneity observed in most cases may promote therapy resistance and underscores the need for precise molecular stratification to improve treatment outcomes.

Indexed as

Biomarkers, TumorCarcinoma, HepatocellularLiver NeoplasmsProteomicsAdultAgedFemaleHumansMaleMiddle AgedSingle-Cell AnalysisTissue Array AnalysisBiomarkers, TumorHCCIntratumoral heterogeneityMultiplexed immunofluorescenceMultispectral imaging

Identifiers

PMID41042332
PMCPMC12647349

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.