Evidence map›Paper›PMID 40175686›Full record

ArticleCommunications medicine2025

Functionally enriched epigenetic clocks reveal tissue-specific discordant aging patterns in individuals with cancer.

Chiara M S Herzog, Elisa Redl, James Barrett, Sepideh Aminzadeh-Gohari, Daniela D Weber, Julia Tevini, Roland Lang, Barbara Kofler, Martin Widschwendter

Abstract read
In one paragraph

Article in Communications medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
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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

9 authors.

Chiara M S HerzogEuropean Translational Oncology Prevention and Screening Institute, Universität Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-1572-498X
Elisa RedlEuropean Translational Oncology Prevention and Screening Institute, Universität Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0001-6540-8443
James BarrettEuropean Translational Oncology Prevention and Screening Institute, Universität Innsbruck, Innsbruck, Austria.
Sepideh Aminzadeh-GohariEuropean Translational Oncology Prevention and Screening Institute, Universität Innsbruck, Innsbruck, Austria.
Daniela D WeberResearch Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, University Hospital of the Paracelsus Medical University, Salzburg, Austria.ORCID http://orcid.org/0000-0002-9825-6674
Julia TeviniResearch Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, University Hospital of the Paracelsus Medical University, Salzburg, Austria.ORCID http://orcid.org/0009-0007-0195-2619
Roland LangDepartment of Dermatology and Allergology, University Hospital of the Paracelsus Medical University, Salzburg, Austria.
Barbara KoflerResearch Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, University Hospital of the Paracelsus Medical University, Salzburg, Austria.ORCID http://orcid.org/0000-0002-1198-4776
Martin WidschwendterEuropean Translational Oncology Prevention and Screening Institute, Universität Innsbruck, Innsbruck, Austria. martin.widschwendter@uibk.ac.at.ORCID http://orcid.org/0000-0002-7778-8380

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 742432Vetenskapsrådet (Swedish Research Council) 2021-02974
6 · The paper itself

Abstract

backgroundAging is a key risk factor for many diseases, including cancer, and a better understanding of its underlying molecular mechanisms may help to prevent, delay, or treat age-related pathologies. Epigenetic alterations such as DNA methylation (DNAme) changes are a hallmark of aging and form the basis of so-called epigenetic clocks, yet their functional relevance and directionality in different organs during disease development is often unclear.

methodsHere, we link cell-specific age-related DNAme changes with three key hallmarks of aging and cancer (senescence, promoter methylation in genes associated with stem cell fate, and dysregulated proliferation) to comprehensively dissect their association with current and future cancer development, carcinogen exposure or preventive measures, and mortality using data in different organs from over 12,510 human and 105 mouse samples, benchmarking against existing epigenetic clocks.

resultsOur findings offer insights into the association of functionally enriched groups of age-related DNAme changes with cancer, identify sites perturbed earliest during carcinogenesis, as well as those distinct between cancer and reprogramming that could inform strategies to prevent teratoma formation upon in vivo reprogramming. Surprisingly, both mouse and human data reveal accelerated aging in breast cancer tissue but decelerated epigenetic aging in some non-cancer surrogate samples from breast cancer patients, in particular cervical samples.

conclusionsThis work provides evidence for discordant systemic tissue aging in breast cancer.

Identifiers

PMID40175686
PMCPMC11965555

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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.