Evidence map›Paper›PMID 34102225›Full record

ReviewExperimental cell research2021

Balancing DNA repair to prevent ageing and cancer.

Eleanor Rachel Stead, Ivana Bjedov

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental cell research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

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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

2 authors at 2 institutions in 1 country.

Eleanor Rachel SteadUCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London, London WC1E 6DD, UK.
Ivana BjedovUCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London, London WC1E 6DD, UK; University College London, Department of Medical Physics and Biomedical Engineering, Malet Place Engineering Building, Gower Street, London WC1E 6BT, UK. Electronic address: i.bjedov@ucl.ac.uk.
CRUK Lung Cancer Centre of Excellence · GBUniversity College London · GB

Funding

Cancer Research UK 28990Cancer Research UK C416/A25145Cancer Research UK C7893/A28990Medical Research Council MR/M02492X/1
6 · The paper itself

Abstract

DNA damage is a constant stressor to the cell. Persistent damage to the DNA over time results in an increased risk of mutation and an accumulation of mutations with age. Loss of efficient DNA damage repair can lead to accelerated ageing phenotypes or an increased cancer risk, and the trade-off between cancer susceptibility and longevity is often driven by the cell's response to DNA damage. High levels of mutations in DNA repair mutants often leads to excessive cell death and stem cell exhaustion which may promote premature ageing. Stem cells themselves have distinct characteristics that enable them to retain low mutation rates. However, when mutations do arise, stem cell clonal expansion can also contribute to age-related tissue dysfunction as well as heightened cancer risk. In this review, we will highlight increasing DNA damage and mutation accumulation as hallmarks common to both ageing and cancer. We will propose that anti-ageing interventions might be cancer preventative and discuss the mechanisms through which they may act.

Indexed as

AgingDNA DamageDNA RepairGenomic InstabilityLongevityNeoplasmsAgeingCancerChromatinDNA damageDNA repairEpigeneticHealthspanLifespanLongevityMutationStem cells

Identifiers

PMID34102225
PMCPMC8361780
OpenAlexW3171652041

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.