Evidence map›Paper›PMID 27106867›Full record

ArticleMolecular cancer research : MCR2016

Oxidative Stress-Induced Protein Damage Inhibits DNA Repair and Determines Mutation Risk and Therapeutic Efficacy.

Elizabeth McAdam, Reto Brem, Peter Karran

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.9field-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

43 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
  2. Characterising the urinary excretion of thymidine dimer photolesions in mice.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Article
  3. Changes in ultraviolet B radiation-induced DNA damage and erythema after oral nicotinamide and polypodium leucotomos in healthy volunteers: an intraindividual controlled trial.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
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  20. Long-wavelength UVA enhances UVB-induced cell death in cultured keratinocytes: DSB formation and suppressed survival pathway.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2021
    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.

Elizabeth McAdamThe Francis Crick Institute, Clare Hall Laboratory, South Mimms, Hertfordshire, United Kingdom.
Reto BremThe Francis Crick Institute, Clare Hall Laboratory, South Mimms, Hertfordshire, United Kingdom.
Peter KarranThe Francis Crick Institute, Clare Hall Laboratory, South Mimms, Hertfordshire, United Kingdom. peter.karran@crick.ac.uk.
The Francis Crick Institute · GB

Funding

Cancer Research UK 11584Cancer Research UK A11584Cancer Research UK A3558
6 · The paper itself

Abstract

unlabelledThe relationship between sun exposure and nonmelanoma skin cancer risk is well established. Solar UV (wavelength 280-400 nm) is firmly implicated in skin cancer development. Nucleotide excision repair (NER) protects against cancer by removing potentially mutagenic DNA lesions induced by UVB (280-320 nm). How the 20-fold more abundant UVA (320-400 nm) component of solar UV radiation increases skin cancer risk is not understood. Here it is demonstrated that the contribution of UVA to the effect of UV radiation on cultured human cells is largely independent of its ability to damage DNA. Instead, the effects of UVA reflect the induction of oxidative stress that causes extensive protein oxidation. Because NER proteins are among those damaged, UVA irradiation inhibits NER and increases the susceptibility of the cells to mutation by UVB. NER inhibition is a common consequence of oxidative stress. Exposure to chemical oxidants, treatment with drugs that deplete cellular antioxidants, and interventions that interfere with glucose metabolism to disrupt the supply of cellular reducing power all inhibit NER. Tumor cells are often in a condition of oxidative stress and one effect of the NER inhibition that results from stress-induced protein oxidation is an increased sensitivity to the anticancer drug cisplatin. IMPLICATIONS: As NER is both a defense against cancer and a significant determinant of cell survival after treatment with anticancer drugs, its attenuation by protein damage under conditions of oxidative stress has implications for both cancer risk and for the effectiveness of anticancer therapy. Mol Cancer Res; 14(7); 612-22. ©2016 AACR.

Indexed as

Cell Line, TumorDNA DamageDNA RepairHeLa CellsHumansKeratinocytesMutagenesisMutationOxidative StressReactive Oxygen SpeciesRisk FactorsUltraviolet RaysReactive Oxygen Species

Identifiers

PMID27106867
PMCPMC4955916
OpenAlexW2341278327

What OpenQuestion holds

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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.