Evidence map›Paper›PMID 38884048›Full record

ArticleAdvanced genetics (Hoboken, N.J.)2024

The Surprising Diversity of UV-Induced Mutations.

Marian F Laughery, Hannah E Wilson, Allysa Sewell, Scott Stevison, John J Wyrick

Abstract read
In one paragraph

Article in Advanced genetics (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. [Chronic skin damage from UV radiation].Dermatologie (Heidelberg, Germany) · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Nanorate sequencing reveals theProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. The Surprising Diversity of UV-Induced Mutations.Advanced genetics (Hoboken, N.J.) · 2024
    Article
  16. Illuminating genome repair by photolyase.Photochemistry and photobiology
    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

5 authors.

Marian F LaugherySchool of Molecular Biosciences Washington State University Pullman WA 99164 USA.
Hannah E WilsonSchool of Molecular Biosciences Washington State University Pullman WA 99164 USA.
Allysa SewellSchool of Molecular Biosciences Washington State University Pullman WA 99164 USA.
Scott StevisonSchool of Molecular Biosciences Washington State University Pullman WA 99164 USA.
John J WyrickSchool of Molecular Biosciences Washington State University Pullman WA 99164 USA.ORCID https://orcid.org/0000-0002-7911-3803

Funding

Genome-wide analysis of the formation and mutagenesis of atypical UV photoproducts in skin cancerR01ES032814 · NIEHS · WASHINGTON STATE UNIVERSITY · PI STEVEN A ROBERTS, John J Wyrick · 2021 to 2026
$5.8M
Regulation of DNA Excision Repair in ChromatinR01ES028698 · NIEHS · WASHINGTON STATE UNIVERSITY · PI John J Wyrick · 2018 to 2026
$2.7M
Identifying recurrent driver mutations in skin cancers by targeted UV damage sequencingR21ES035139 · NIEHS · WASHINGTON STATE UNIVERSITY · PI WYRICK, JOHN J · 2023 to 2024
$449k
NIEHS NIH HHS R01 ES028698NIEHS NIH HHS R01 ES032814NIEHS NIH HHS R21 ES035139
6 · The paper itself

Abstract

Ultraviolet (UV) light is the most pervasive environmental mutagen and the primary cause of skin cancer. Genome sequencing of melanomas and other skin cancers has revealed that the vast majority of somatic mutations in these tumors are cytosine-to-thymine (C>T) substitutions in dipyrimidine sequences, which, together with tandem CC>TT substitutions, comprise the canonical UV mutation "signature". These mutation classes are caused by DNA damage directly induced by UV absorption, namely cyclobutane pyrimidine dimers (CPDs) or 6-4 pyrimidine-pyrimidone photoproducts (6-4PP), which form between neighboring pyrimidine bases. However, many of the key driver mutations in melanoma do not fit this mutation signature, but instead are caused by T>A, T>C, C>A, or AC>TT substitutions, frequently occurring in non-dipyrimidine sequence contexts. This article describes recent studies indicating that UV light causes a more diverse spectrum of mutations than previously appreciated, including many of the mutation classes observed in melanoma driver mutations. Potential mechanisms for these diverse mutation signatures are discussed, including UV-induced pyrimidine-purine photoproducts and indirect DNA damage induced by UVA light. Finally, the article reviews recent findings indicating that human DNA polymerase eta normally suppresses these non-canonical UV mutation classes, which can potentially explain why canonical C>T substitutions predominate in human skin cancers.

Indexed as

atypical photoproductsDNA repairreactive oxygen speciesskin cancerultraviolet lightUVA

Identifiers

PMID38884048
PMCPMC11170076

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.