Evidence map›Paper›PMID 42769788›Full record

ReviewOncology research2026

Cholesterol Metabolism in Cancer Patients: Mechanisms, Treatment-Related Effects, and Cardio-Oncology Management.

Mariagrazia Piscione, Barbara Pala, Francesco Cribari, Paola Gualtieri, Dario Gaudio, Marco Alfonso Perrone, Laura Di Renzo

Abstract readReview
In one paragraph

Review in Oncology research, 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

7 authors.

Mariagrazia PiscioneSantissima Annuziata Hospital, Via dei Vestini, Chieti, Italy.
Barbara PalaPhD School of Applied Medical-surgical sciences, Tor Vergata University of Rome, Via Montpellier 1, Rome, Italy.
Francesco CribariUOC Cardiologia, Ospedale IDI-IRCCS, Rome, Italy.
Paola GualtieriSection of Clinical Nutrition and Nutrigenomics, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Via Montpellier 1, Rome, Italy.
Dario GaudioFondazione Policlinico Campus Bio-Medico, University of Rome, Via Alvaro del Portillo 200, Rome, Italy.
Marco Alfonso PerroneDivision of Cardiology, Tor Vergata University of Rome, Via Montpellier 1, Rome, Italy.
Laura Di RenzoSection of Clinical Nutrition and Nutrigenomics, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Via Montpellier 1, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholesterol metabolism is central to cancer biology, influencing tumour initiation, progression, and therapeutic response, while contributing to the increased cardiovascular risk observed in cancer patients. Epidemiological studies investigating the relationship between circulating cholesterol levels and cancer risk have yielded conflicting results, reflecting substantial biological heterogeneity, tumour-specific metabolic demands, and methodological biases such as reverse causality. At the cellular level, malignant cells exhibit elevated cholesterol uptake and synthesis to sustain membrane biogenesis, lipid raft-dependent oncogenic signalling, and rapid proliferation. Cholesterol and its oxidized derivatives further modulate inflammation, angiogenesis, immune evasion, and key signalling pathways. Anticancer therapies profoundly disrupt lipid homeostasis; conventional chemotherapies, targeted therapies, hormone-modulating agents, and immunotherapies can induce dyslipidaemia and accelerate atherosclerotic disease, thereby contributing to long-term morbidity in cancer survivors. Conversely, lipid-lowering therapies-particularly statins-have emerged as pivotal tools in cardio-oncology, primarily for cardiovascular protection. Beyond this role, growing evidence suggests potential adjunctive antitumor effects mediated through inhibition of the mevalonate pathway, blockade of oncogenic signalling, and modulation of the tumour microenvironment. Novel agents, including ezetimibe, bempedoic acid, and proprotein convertase subtilisin-kexin type 9 inhibitors, provide additional therapeutic options, with emerging evidence supporting their immunomodulatory and anticancer properties, especially in combination with immune checkpoint inhibitors. Cholesterol metabolism plays a critical role in both CV disease and cancer biology, with growing evidence suggesting a complex bidirectional relationship between lipid homeostasis and tumour development. In addition, several anticancer therapies may profoundly affect lipid metabolism, thereby contributing to CV risk in cancer patients. The aim of this review is to provide a comprehensive overview of the interplay between cholesterol metabolism and cancer, to summarize the lipid-modifying effects of anticancer therapies, and to discuss the potential role of lipid-lowering strategies within the evolving framework of cardio-oncology care.

Indexed as

Cardiovascular DiseasesCholesterolNeoplasmsAnimalsAntineoplastic AgentsHumansLipid MetabolismAntineoplastic AgentsCholesterolcancer progressioncardio-oncologyCholesterol metabolismdyslipidaemialipid-lowering therapies

Identifiers

PMID42769788
PMCPMC13591320

What OpenQuestion holds

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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.