Evidence map›Paper›PMID 42067907›Full record

ArticleCardio-oncology (London, England)2026

The role of angiotensin II in cardiovascular disease-induced cancer growth.

Benji van Berlo, Pierangela Esposito, Alessandra Greco, Charles X L van Assche, Tine Bruyns, Birgit Van Asbroeck, Celine Civati, Ronny Mohren, Berta Cillero-Pastor, Pieter-Jan Guns and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardio-oncology (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Benji van BerloLaboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium. Benji.vanberlo@uantwerpen.be.
Pierangela Esposito *Laboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Alessandra Greco *Laboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Charles X L van AsscheDivision M4I - Imaging Mass Spectrometry (IMS), Faculty of Health, Medicine and Life Sciences, Maastricht MultiModal Molecular Imaging Institute, Maastricht University, Universiteitssingel 50, Maastricht, 6229 ER, The Netherlands.
Tine BruynsLaboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Birgit Van AsbroeckLaboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Celine CivatiLaboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Ronny MohrenDivision M4I - Imaging Mass Spectrometry (IMS), Faculty of Health, Medicine and Life Sciences, Maastricht MultiModal Molecular Imaging Institute, Maastricht University, Universiteitssingel 50, Maastricht, 6229 ER, The Netherlands.
Berta Cillero-PastorDivision M4I - Imaging Mass Spectrometry (IMS), Faculty of Health, Medicine and Life Sciences, Maastricht MultiModal Molecular Imaging Institute, Maastricht University, Universiteitssingel 50, Maastricht, 6229 ER, The Netherlands.
Pieter-Jan Guns *Laboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Gilles W De Keulenaer *Laboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.
Vincent F M Segers *Laboratory of Physiopharmacology, Faculty of Medicine and Health Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, UA CDE D.T.218, Antwerp, B-2610, Belgium.

Funding

Horizon 2020 858070
6 · The paper itself

Abstract

backgroundThe higher incidence of cancer in patients with cardiovascular disease (CVD) has historically been explained by shared risk factors. Recent studies suggest, however, a causal relationship. Nevertheless, the mechanisms of CVD-induced cancer are incompletely understood. Here, we hypothesize that angiotensin II (ANGII) links CVD and increased cancer growth.

objectiveWe investigated the impact of ANGII-induced CVD on cancer growth in vivo, differentiating between a direct effect of ANGII on tumor cells or indirect effects secondary to CVD.

methodsThe effect of ANGII on cancer growth was studied in C57BL/6J mice with cancer. Cancer was either induced by subcutaneous injection of Lewis lung carcinoma (LLC) cells, MC38 colon cancer cells, or by genetic susceptibility (APC

resultsHigh dose ANGII-treatment induced left ventricle (LV) hypertrophy and cardiac fibrosis, and enhanced growth of injected tumor cells, but only when LCC tumor cells with high expression of AT1 were used, and when these cells were injected during ANGII treatment. ANGII did not increase cancer growth when LCC cells were injected after halting ANGII treatment, or when MC38 tumor cells with low AT1 levels were used. ANGII also increased the number of intestinal polyps in APC

conclusionThis study indicates that ANGII has direct effects on cancer growth, warranting further research into the role of an activated renin-angiotensin-aldosterone-system (RAAS) as a mechanistic link between CVD and cancer growth in AT1-positive tumors.

Indexed as

Angiotensin IIAT1CancerCardiovascular diseaseRAAS

Identifiers

PMID42067907
PMCPMC13277031

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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.