Evidence map›Paper›PMID 30868047›Full record

ReviewChemistryOpen2019

Oxidation Chemistry of DNA and p53 Tumor Suppressor Gene.

Di Jiang, James F Rusling

Open access · goldAbstract readReview
In one paragraph

Review in ChemistryOpen, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. The Influence of Oxidized Imino-Allantoin in the Presence ofInternational journal of molecular sciences · 2024
    Article
  7. Review
  8. Mapping the diffusion pattern ofScientific reports · 2023
    Article
  9. Article
  10. EPR Study of KOAntioxidants (Basel, Switzerland) · 2021
    Article
  11. Review
  12. Review
  13. Review
  14. 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 at 1 institution in 2 countries.

Di JiangDepartment of Chemistry University of Connecticut Storrs CT 06269 United States.
James F RuslingDepartment of Chemistry University of Connecticut Storrs CT 06269 United States.ORCID 0000-0002-6117-3306
University of Connecticut · US

Funding

ELECTROCATALYTIC STUDIES OF TOXIC POLLUTANT ACTIVATIONR01ES003154 · NIEHS · UNIVERSITY OF CONNECTICUT STORRS · PI RUSLING, JAMES F. · 1985 to 2018
$6.1M
NIEHS NIH HHS R01 ES003154
6 · The paper itself

Abstract

The chemistry of DNA and its repair selectivity control the influence of genomic oxidative stress on the development of serious disorders such as cancer and heart diseases. DNA is oxidized by endogenous reactive oxygen species (ROS) in vivo or in vitro as a result of high energy radiation, non-radiative metabolic processes, and other consequences of oxidative stress. Some oxidations of DNA and tumor suppressor gene p53 are thought to be mutagenic when not repaired. For example, site-specific oxidations of p53 tumor suppressor gene may lead to cancer-related mutations at the oxidation site codon. This review summarizes the research on the primary products of the most easily oxidized nucleobase guanine (G) when different oxidation methods are used. Guanine is by far the most oxidized DNA base. The primary initial oxidation product of guanine for most, but not all, pathways is 8-oxoguanine (8-oxoG). With an oxidation potential much lower than G, 8-oxoG is readily susceptible to further oxidation, and the products often depend on the oxidants. Specific products may control the types of subsequent mutations, but mediated by gene repair success. Site-specific oxidations of p53 tumor suppressor gene have been reported at known mutation hot spots, and the codon sites also depend on the type of oxidants. Modern methodologies using LC-MS/MS for codon specific detection and identification of oxidation sites are summarized. Future work aimed at understanding DNA oxidation in nucleosomes and interactions between DNA damage and repair is needed to provide a better picture of how cancer-related mutations arise.

Indexed as

DNA mutationsDNA oxidationLC–MS/MSoxidative productsp53 tumor suppressor gene

Identifiers

PMID30868047
PMCPMC6398102
OpenAlexW2917089372

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.