Evidence map›Paper›PMID 34463773›Full record

ReviewCellular and molecular life sciences : CMLS2021

Genome-wide mapping of genomic DNA damage: methods and implications.

Stefano Amente, Giovanni Scala, Barbara Majello, Somaiyeh Azmoun, Helen G Tempest, Sanjay Premi, Marcus S Cooke

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

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  4. Integrating multi-omics data for next-generation cancer research and precision medicine.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

7 authors at 4 institutions in 2 countries.

Stefano AmenteDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples 'Federico II', Naples, Italy.
Giovanni ScalaDepartment of Biology, University of Naples 'Federico II', Naples, Italy.
Barbara MajelloDepartment of Biology, University of Naples 'Federico II', Naples, Italy.
Somaiyeh AzmounDepartment of Environmental Health Sciences, Florida International University, Miami, FL, 33199, USA.
Helen G TempestDepartment of Human and Molecular Genetics, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, 33199, USA.
Sanjay PremiDepartment of Tumor Biology, Moffitt Cancer Centre and Research Institute, Tampa, FL, USA.
Marcus S CookeOxidative Stress Group, Department of Cell Biology, Microbiology, and Molecular Biology, University of South Florida, 4202 East Fowler Avenue, ISA 6207, Tampa, 33620, USA. cookem@usf.edu.ORCID http://orcid.org/0000-0003-0369-862X
University of Naples Federico II · ITFlorida International University · USMoffitt Cancer Center · USUniversity of South Florida · US

Funding

Urinary DNA Adductomics for the Assessment of Exposure to Cancer Risk FactorsR01ES030557 · NIEHS · UNIVERSITY OF SOUTH FLORIDA · PI COOKE, MARCUS STANLEY, HU, CHIUNG-WEN · 2019 to 2023
$1.7M
Genomic instability, susceptibility to oxidative stress and cellular senescenceR15ES027196 · NIEHS · FLORIDA INTERNATIONAL UNIVERSITY · PI COOKE, MARCUS STANLEY · 2017 to 2017
$366k
association for international cancer research IG 23066National Institute of Environmental Health Sciences (US) R01ES030557NIEHS NIH HHS R01 ES030557NIEHS NIH HHS R15 ES027196NIEHS NIH HHS R15ES027196pon aim E69F19000070001por campania FESR 2014-2020 "SATIN"
6 · The paper itself

Abstract

Exposures from the external and internal environments lead to the modification of genomic DNA, which is implicated in the cause of numerous diseases, including cancer, cardiovascular, pulmonary and neurodegenerative diseases, together with ageing. However, the precise mechanism(s) linking the presence of damage, to impact upon cellular function and pathogenesis, is far from clear. Genomic location of specific forms of damage is likely to be highly informative in understanding this process, as the impact of downstream events (e.g. mutation, microsatellite instability, altered methylation and gene expression) on cellular function will be positional-events at key locations will have the greatest impact. However, until recently, methods for assessing DNA damage determined the totality of damage in the genomic location, with no positional information. The technique of "mapping DNA adductomics" describes the molecular approaches that map a variety of forms of DNA damage, to specific locations across the nuclear and mitochondrial genomes. We propose that integrated comparison of this information with other genome-wide data, such as mutational hotspots for specific genotoxins, tumour-specific mutation patterns and chromatin organisation and transcriptional activity in non-cancerous lesions (such as nevi), pre-cancerous conditions (such as polyps) and tumours, will improve our understanding of how environmental toxins lead to cancer. Adopting an analogous approach for non-cancer diseases, including the development of genome-wide assays for other cellular outcomes of DNA damage, will improve our understanding of the role of DNA damage in pathogenesis more generally.

Indexed as

AnimalsChromosome MappingDNADNA DamageGenomeGenome-Wide Association StudyGenomicsHumansMutationNeoplasmsDNAAdductomicsDNA damageDNA repairGenomic instabilityMappingNext-generation sequencing

Identifiers

PMID34463773
PMCPMC8558167
OpenAlexW3196885070

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.