Evidence map›Paper›PMID 38519484›Full record

ArticleNature communications2024

Cancer cell genetics shaping of the tumor microenvironment reveals myeloid cell-centric exploitable vulnerabilities in hepatocellular carcinoma.

Christel F A Ramirez, Daniel Taranto, Masami Ando-Kuri, Marnix H P de Groot, Efi Tsouri, Zhijie Huang, Daniel de Groot, Roelof J C Kluin, Daan J Kloosterman, Joanne Verheij and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Metastasis-promoting functions of myeloid cells.Cancer metastasis reviews · 2025
    Review
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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

13 authors at 3 institutions in 2 countries.

Christel F A Ramirez *Division of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Daniel Taranto *Division of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Masami Ando-Kuri *Division of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Marnix H P de GrootDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Efi TsouriDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Zhijie HuangState Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, 510060, PR China.
Daniel de GrootDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Roelof J C KluinGenomics Core facility, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Daan J KloostermanDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0003-1082-070X
Joanne VerheijDepartment of Pathology, Cancer Center Amsterdam, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Jing XuDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0002-4713-2807
Serena VegnaDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands. s.vegna@nki.nl.ORCID http://orcid.org/0000-0003-0518-9319
Leila AkkariDivision of Tumor Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands. l.akkari@nki.nl.ORCID http://orcid.org/0000-0001-5479-641X
The Netherlands Cancer Institute · NLSun Yat-sen University · CNAmsterdam University Medical Centers · NL

Funding

KWF Kankerbestrijding (Dutch Cancer Society) 12049KWF Kankerbestrijding (Dutch Cancer Society) 13476
6 · The paper itself

Abstract

Myeloid cells are abundant and plastic immune cell subsets in the liver, to which pro-tumorigenic, inflammatory and immunosuppressive roles have been assigned in the course of tumorigenesis. Yet several aspects underlying their dynamic alterations in hepatocellular carcinoma (HCC) progression remain elusive, including the impact of distinct genetic mutations in shaping a cancer-permissive tumor microenvironment (TME). Here, in newly generated, clinically-relevant somatic female HCC mouse models, we identify cancer genetics' specific and stage-dependent alterations of the liver TME associated with distinct histopathological and malignant HCC features. Mitogen-activated protein kinase (MAPK)-activated, Nras

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansImmunosuppressive AgentsInflammationMiceMitogen-Activated Protein KinasesMyeloid CellsTumor MicroenvironmentVascular Endothelial Growth Factor AGranulocyte-Macrophage Colony-Stimulating FactorImmunosuppressive AgentsMitogen-Activated Protein KinasesVascular Endothelial Growth Factor A

Identifiers

PMID38519484
PMCPMC10959959
OpenAlexW4393067722

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.