Evidence map›Paper›PMID 22156741›Full record

ReviewGerontology2012

Measuring genome instability in aging - a mini-review.

Wenge Li, Jan Vijg

Abstract readReview
In one paragraph

Review in Gerontology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Flavonoids-Natural Gifts to Promote Health and Longevity.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Expression of progerin does not result in an increased mutation rate.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017
    Article
  10. Article
  11. Article
  12. DNA Damage, DNA Repair, Aging, and Neurodegeneration.Cold Spring Harbor perspectives in medicine · 2015
    Review
  13. Article
  14. Alterations in the mutagenicity and mutation spectrum induced by benzo[a]pyrene instilled in the lungs of gpt delta mice of various ages.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2015
    Article
  15. Review
  16. Article
  17. Review
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.

Wenge LiDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Jan Vijg

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
Single-Cell Functional GenomicsR01AG034421 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI VIJG, JAN · 2009 to 2012
$1.4M
Direct Somatic Mutation Analysis Through SequencingR21ES019520 · NIEHS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI VIJG, JAN · 2011 to 2012
$457k
NIA NIH HHS P01 AG017242NIA NIH HHS P01AG17242NIA NIH HHS R01 AG034421NIA NIH HHS R01AG034421NIEHS NIH HHS R21 ES019520NIEHS NIH HHS R21ES019520
6 · The paper itself

Abstract

backgroundThere is mounting evidence for an age-dependent accumulation of somatic mutations as a result of the inherent imperfection of DNA replication and repair. A possible age-related decline in genome maintenance systems may exacerbate this age-related loss of genome integrity. A review of the current methods of mutation detection is timely in view of the lack of insight as to the magnitude of somatic mutation accumulation, the types of mutations that accumulate, and their functional consequences.

objectiveIn this paper we review the current methods for measuring genome instability in organisms during aging or in relation to life span.

methodsThe review is based on established and novel concepts from the existing literature, with some examples from our own laboratory.

resultsStudies using cytogenetic assays and endogenous or transgenic mutation reporter assays provide strong evidence for age-related increases of different types of mutations in animals and humans during aging. This increase in DNA mutations is tissue-specific and also differs between species.

conclusionToday, our knowledge of somatic mutation profiles in aging is mainly derived from cytogenetics and the use of endogenous and transgenic mutation reporter assays. The emergence of new approaches, most notably massively parallel sequencing, will give us deeper insight into the nature of spontaneous genome instability and its possible causal relationship to aging and age-related disease.

Indexed as

Genomic InstabilityAgingAneuploidyAnimalsAnimals, Genetically ModifiedDNA DamageDNA Mutational AnalysisDNA RepairGenes, ReporterHumansModels, GeneticMutation

Identifiers

PMID22156741
PMCPMC3696364

What OpenQuestion holds

Textmetadata
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.