Evidence map›Paper›PMID 29723708›Full record

ArticleDNA repair

Broad spectrum detection of DNA damage by Repair Assisted Damage Detection (RADD).

Nathaniel W Holton, Yuval Ebenstein, Natalie R Gassman

Open access · greenAbstract read
In one paragraph

Article in DNA repair. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Acute Heat Exposure Upregulates Zebra Finch Physiology While Avoiding DNA Damage Across Both Sexes.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2026
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  9. Poly ADP-ribose signaling is dysregulated in Huntington disease.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  11. Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024
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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

3 authors at 2 institutions in 2 countries.

Nathaniel W HoltonDepartment of Oncologic Sciences, University of South Alabama Mitchell Cancer Institute, Mobile, AL, 36604, USA. Electronic address: nwholton@health.southalabama.edu.
Yuval EbensteinSchool of Chemistry, Center for Nanoscience and Nanotechnology, Center for Light-Matter Interaction, Raymond and Beverly Sackler Faculty of Exact Sciences, Tel Aviv University, Tel Aviv, Israel. Electronic address: uv@post.tau.ac.il.
Natalie R GassmanDepartment of Oncologic Sciences, University of South Alabama Mitchell Cancer Institute, Mobile, AL, 36604, USA. Electronic address: nrgassman@health.southalabama.edu.
USA Mitchell Cancer Institute · USTel Aviv University · IL

Funding

Co-detection of DNA adducts and methylation sites as predictive biomarkers for exposuresR21ES028015 · NIEHS · UNIVERSITY OF SOUTH ALABAMA · PI EBENSTEIN, YUVAL, GASSMAN, NATALIE ROSE · 2017 to 2018
$389k
NIEHS NIH HHS R21 ES028015
6 · The paper itself

Abstract

Environmental exposures, reactive by-products of cellular metabolism, and spontaneous deamination events result in a spectrum of DNA adducts that if un-repaired threaten genomic integrity by inducing mutations, increasing instability, and contributing to the initiation and progression of cancer. Assessment of DNA adducts in cells and tissues is critical for genotoxic and carcinogenic evaluation of chemical exposure and may provide insight into the etiology of cancer. Numerous methods to characterize the formation of DNA adducts and their retention for risk assessment have been developed. However, there are still significant drawbacks to the implementation and wide-spread use of these methods, because they often require a substantial amount of biological sample, highly specialized expertise and equipment, and depending on technique, may be limited to the detection and quantification of only a handful of DNA adducts at a time. There is a pressing need for high throughput, easy to implement assays that can assess a broad spectrum of DNA lesions, allowing for faster evaluation of chemical exposures and assessment of the retention of adducts in biological samples. Here, we describe a new methodology, Repair Assisted Damage Detection (RADD), which utilizes a DNA damage processing repair enzyme cocktail to detect and modify sites of DNA damage for a subsequent gap filling reaction that labels the DNA damage sites. This ability to detect and label a broad spectrum of DNA lesions within cells, offers a novel and easy to use tool for assessing levels of DNA damage in cells that have been exposed to environmental agents or have natural variations in DNA repair capacity.

Indexed as

Cell Line, TumorDNA AdductsDNA RepairEnvironmental ExposureHumansMutagenicity TestsDNA AdductsConfocal microscopyDNA adductDNA damage detectionDNA repairFluorescence

Identifiers

PMID29723708
PMCPMC6375075
OpenAlexW2800975962

What OpenQuestion holds

Textmetadata
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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.