Evidence map›Paper›PMID 35726685›Full record

ReviewMolecular oncology2022

The sculpting of somatic mutational landscapes by evolutionary forces and their impacts on aging-related disease.

Fabio Marongiu, James DeGregori

Open access · goldAbstract readReview
In one paragraph

Review in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 7% of its field
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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Integrated Clinicogenomic Risk Modeling for Metachronous Second Primary Cancers.medRxiv : the preprint server for health sciences · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. The Aging-Cancer Cycle: Mechanisms and Opportunities for Intervention.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023
    Article
  19. Ageing as a software design flaw.Genome biology · 2023
    Review
  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 at 2 institutions in 2 countries.

Fabio MarongiuDepartment of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.ORCID 0000-0001-5860-4227
James DeGregoriDepartment of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.ORCID 0000-0002-1287-1976
University of Cagliari · ITUniversity of Colorado Cancer Center · US

Funding

Preventing Cognitive Decline and Dementia Among Older Chinese Immigrants: The Role of Activity, Engagement, Immigration Experience, and Neighborhood EnvironmentsR01AG067548 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TANG, FENGYAN · 2020 to 2023
$2.2M
BLRD VA I01 BX004495NIA NIH HHS R01 AG067548
6 · The paper itself

Abstract

Aging represents the major risk factor for the development of cancer and many other diseases. Recent findings show that normal tissues become riddled with expanded clones that are frequently driven by cancer-associated mutations in an aging-dependent fashion. Additional studies show how aged tissue microenvironments promote the initiation and progression of malignancies, while young healthy tissues actively suppress the outgrowth of malignant clones. Here, we discuss conserved mechanisms that eliminate poorly functioning or potentially malignant cells from our tissues to maintain organismal health and fitness. Natural selection acts to preserve tissue function and prevent disease to maximize reproductive success but these mechanisms wane as reproduction becomes less likely. The ensuing age-dependent tissue decline can impact the shape and direction of clonal somatic evolution, with lifestyle and exposures influencing its pace and intensity. We also consider how aging- and exposure-dependent clonal expansions of "oncogenic" mutations might both increase cancer risk late in life and contribute to tissue decline and non-malignant disease. Still, we can marvel at the ability of our bodies to avoid cancers and other diseases despite the accumulation of billions of cells with cancer-associated mutations.

Indexed as

Clonal EvolutionNeoplasmsAgedAgingClone CellsHumansMutationTumor Microenvironmentagingclonal hematopoiesislife-history theoryNOTCH1p53somatic evolution

Identifiers

PMID35726685
PMCPMC9490148
OpenAlexW4283266377

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.