Evidence map›Paper›PMID 27582430›Full record

ReviewBiochemistry2016

Excessive Reactive Oxygen Species and Exotic DNA Lesions as an Exploitable Liability.

Safnas F AbdulSalam, Fathima Shazna Thowfeik, Edward J Merino

Open access · greenAbstract readReview
In one paragraph

Review in Biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Photodynamic Therapy for Atherosclerosis.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Oxidative medicine and cellular longevity · 2022
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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 1 institution in 1 country.

Safnas F AbdulSalamDepartment of Chemistry, University of Cincinnati , 404 Crosley Tower, Cincinnati, Ohio 45221-0172, United States.
Fathima Shazna ThowfeikDepartment of Chemistry, University of Cincinnati , 404 Crosley Tower, Cincinnati, Ohio 45221-0172, United States.
Edward J MerinoDepartment of Chemistry, University of Cincinnati , 404 Crosley Tower, Cincinnati, Ohio 45221-0172, United States.
University of Cincinnati · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Conferring in vivo metabolic resistance to a highly selective anti-AML agentR21CA185370 · NCI · UNIVERSITY OF CINCINNATI · PI MERINO, EDWARD J · 2014 to 2015
$370k
NCATS NIH HHS UL1 TR001425NCI NIH HHS R21 CA185370
6 · The paper itself

Abstract

Although the terms "excessive reactive oxygen species (ROS)" and "oxidative stress" are widely used, the implications of oxidative stress are often misunderstood. ROS are not a single species but a variety of compounds, each with unique biochemical properties and abilities to react with biomolecules. ROS cause activation of growth signals through thiol oxidation and may lead to DNA damage at elevated levels. In this review, we first discuss a conceptual framework for the interplay of ROS and antioxidants. This review then describes ROS signaling using FLT3-mediated growth signaling as an example. We then focus on ROS-mediated DNA damage. High concentrations of ROS result in various DNA lesions, including 8-oxo-7,8-dihydro-guanine, oxazolone, DNA-protein cross-links, and hydantoins, that have unique biological impacts. Here we delve into the biochemistry of nine well-characterized DNA lesions. Within each lesion, the types of repair mechanisms, the mutations induced, and their effects on transcription and replication are discussed. Finally, this review will discuss biochemically inspired implications for cancer therapy. Several teams have put forward designs to harness the excessive ROS and the burdened DNA repair systems of tumor cells for treating cancer. We discuss inhibition of the antioxidant system, the targeting of DNA repair, and ROS-activated prodrugs.

Indexed as

DNA DamageAntineoplastic AgentsHumansReactive Oxygen SpeciesSignal TransductionAntineoplastic AgentsReactive Oxygen Species

Identifiers

PMID27582430
PMCPMC5586498
OpenAlexW2514373129

What OpenQuestion holds

Textmetadata
LicenceTDM
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.