Evidence map›Paper›PMID 39444444›Full record

ReviewEvolutionary applications2024

When Do Tumours Develop? Neoplastic Processes Across Different Timescales: Age, Season and Round the Circadian Clock.

Margaux Bieuville, Antoine M Dujon, Nynke Raven, Beata Ujvari, Pascal Pujol, Zahra Eslami-S, Catherine Alix Panabières, Jean-Pascal Capp, Frédéric Thomas

Abstract readReview
In one paragraph

Review in Evolutionary applications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

9 authors.

Margaux BieuvilleCREEC (CREES), Unité Mixte de Recherches IRD 224-CNRS 5290-Université de Montpellier Montpellier France.ORCID https://orcid.org/0000-0002-4741-5575
Antoine M DujonSchool of Life and Environmental Sciences Deakin University Waurn Ponds Victoria Australia.
Nynke RavenSchool of Life and Environmental Sciences Deakin University Waurn Ponds Victoria Australia.
Beata UjvariCREEC (CREES), Unité Mixte de Recherches IRD 224-CNRS 5290-Université de Montpellier Montpellier France.ORCID https://orcid.org/0000-0003-2391-2988
Pascal PujolCREEC (CREES), Unité Mixte de Recherches IRD 224-CNRS 5290-Université de Montpellier Montpellier France.
Zahra Eslami-SCREEC (CREES), Unité Mixte de Recherches IRD 224-CNRS 5290-Université de Montpellier Montpellier France.
Catherine Alix PanabièresCREEC (CREES), Unité Mixte de Recherches IRD 224-CNRS 5290-Université de Montpellier Montpellier France.ORCID https://orcid.org/0000-0002-6401-2903
Jean-Pascal CappToulouse Biotechnology Institute University of Toulouse, INSA, CNRS, INRAE Toulouse France.ORCID https://orcid.org/0000-0002-6470-079X
Frédéric ThomasCREEC (CREES), Unité Mixte de Recherches IRD 224-CNRS 5290-Université de Montpellier Montpellier France.ORCID https://orcid.org/0000-0003-2238-1978

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While it is recognised that most, if not all, multicellular organisms harbour neoplastic processes within their bodies, the timing of when these undesirable cell proliferations are most likely to occur and progress throughout the organism's lifetime remains only partially documented. Due to the different mechanisms implicated in tumourigenesis, it is highly unlikely that this probability remains constant at all times and stages of life. In this article, we summarise what is known about this variation, considering the roles of age, season and circadian rhythm. While most studies requiring that level of detail be done on humans, we also review available evidence in other animal species. For each of these timescales, we identify mechanisms or biological functions shaping the variation. When possible, we show that evolutionary processes likely played a role, either directly to regulate the cancer risk or indirectly through trade-offs. We find that neoplastic risk varies with age in a more complex way than predicted by early epidemiological models: rather than resulting from mutations alone, tumour development is dictated by tissue- and age-specific processes. Similarly, the seasonal cycle can be associated with risk variation in some species with life-history events such as sexual competition or mating being timed according to the season. Lastly, we show that the circadian cycle influences tumourigenesis in physiological, pathological and therapeutic contexts. We also highlight two biological functions at the core of these variations across our three timescales: immunity and metabolism. Finally, we show that our understanding of the entanglement between tumourigenic processes and biological cycles is constrained by the limited number of species for which we have extensive data. Improving our knowledge of the periods of vulnerability to the onset and/or progression of (malignant) tumours is a key issue that deserves further investigation, as it is key to successful cancer prevention strategies.

Indexed as

agecircadian rhythmevolutionneoplasia riskseasonsenescence

Identifiers

PMID39444444
PMCPMC11496201

What OpenQuestion 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 OpenQuestion graph.