Evidence map›Paper›PMID 23140366›Full record

ReviewAnnual review of physiology2013

Aging, cellular senescence, and cancer.

Judith Campisi

2 registry-linked trialsAbstract readReview
In one paragraph

Review in Annual review of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 1,739 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,739citing papers in PubMed, 2 pooled it
–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.

NCT02451774 phase2 / phase3unknown statusnot on this mapstarted 2015, after this paper: background citation

Safety and efficacy of pentoxifylline versus placebo administered as apoptosis inductor during remission induction phase of pediatric patients with acute lymphoblastic leukemia

TypeinterventionalSponsorRamón Óscar González-Ramella, Ph.DRan2015 to 2020Enrolled44ConditionsAcute Lymphoblastic LeukemiaArmsPentoxifylline Plus Chemotherapy, Placebo Plus Chemotherapy
NCT04693442 unknown statusnot on this mapstarted 2016, after this paper: background citation

A Multi-centre, Prospective Study to Examine the Relationship Between Neutrophil Function and Sepsis in Adults and Children With Severe Thermal Injuries

TypeobservationalSponsorUniversity Hospital Birmingham NHS Foundation TrustRan2016 to 2022Enrolled245ConditionsBurnsArmstaking of blood, urine and blood samples and objective scar assessment
3 · Its place in the literature

Who cites it

1,739 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Cell-cycle genes in the mussel Mytilus galloprovincialis are cued by aerial heat stress in a fluctuating tidal environment.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Imaging the hallmarks of cancer.Nature reviews. Cancer · 2026
    Review
  19. Review
  20. Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review

1,679 more citing papers are in PubMed but not listed here.

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

1 author.

Judith CampisiBuck Institute for Research on Aging, Novato, California 94945, USA. jcampisi@buckinstitute.org

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
Systems Biology and Bioinformatics CoreP01AG041122 · NIA · MAYO CLINIC ROCHESTER · PI CAMPISI, JUDITH · 2012 to 2016
$9.8M
CELLULAR SENESCENCE AND CONTROL OF GENE EXPRESSIONR37AG009909 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI CAMPISI, JUDITH · 1995 to 2015
$7.6M
NIA NIH HHS P01 AG017242NIA NIH HHS P01 AG041122NIA NIH HHS R37 AG009909
6 · The paper itself

Abstract

For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.

Indexed as

AgingAnimalsCellular SenescenceDisease Models, AnimalDNA DamageHumansNeoplasmsStress, Physiological

Identifiers

PMID23140366
PMCPMC4166529

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.