Evidence map›Paper›PMID 40038418›Full record

ReviewNature aging2025

The complex interplay between aging and cancer.

Lucrezia A Trastus, Fabrizio d'Adda di Fagagna

Abstract readReview
In one paragraph

Review in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The long-lived immune system of centenarians.Nature reviews. Immunology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Chromatin accessibility regulates age-dependent nuclear mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  16. Review
  17. Article
  18. Aging-associated differences in mammary tumor-initiating populations and immune evasion pathways in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  19. Article
  20. 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

2 authors.

Lucrezia A TrastusIFOM ETS-the AIRC Institute of Molecular Oncology, Milan, Italy. lucrezia.trastus@ifom.eu.ORCID http://orcid.org/0000-0002-2280-3854
Fabrizio d'Adda di FagagnaIFOM ETS-the AIRC Institute of Molecular Oncology, Milan, Italy. fabrizio.dadda@ifom.eu.ORCID http://orcid.org/0000-0002-9603-5966

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) 21091Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) 21762Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) 28211Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) 30471European Commission (EC) CN3European Commission (EC) PE8Fondazione Italiana di Ricerca per la Sclerosi Laterale Amiotrofica (Italian Research Foundation for ALS) FG_24_2020Fondazione Telethon (Telethon Foundation) GMR23T2007Ministero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) 2020CXFL4TMinistero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) 2022R7LH5TRegione Lombardia (Region of Lombardy) DSB.AD004.294Regione Lombardia (Region of Lombardy) EJPRD19-206, GA 825575
6 · The paper itself

Abstract

Cancer is an age-related disease, but the interplay between cancer and aging is complex and their shared molecular drivers are deeply intertwined. This Review provides an overview of how different biological pathways affect cancer and aging, leveraging evidence mainly derived from animal studies. We discuss how genome maintenance and accumulation of DNA mutations affect tumorigenesis and tissue homeostasis during aging. We describe how age-related telomere dysfunction and cellular senescence intricately modulate tumor development through mechanisms involving genomic instability and inflammation. We examine how an aged immune system and chronic inflammation shape tumor immunosurveillance, fueling DNA damage and cellular senescence. Finally, as animal models are important to untangling the relative contributions of these aging-modulated pathways to cancer progression and to test interventions, we discuss some of the limitations of physiological and accelerated aging models, aiming to improve experimental designs and enhance translation.

Indexed as

AgingNeoplasmsAnimalsCellular SenescenceDNA DamageGenomic InstabilityHumansInflammationTelomere

Identifiers

PMID40038418
PMCPMC7618899

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.