Evidence map›Paper›PMID 32188867›Full record

ArticleScientific reports2020

Exome sequencing identifies novel mutation signatures of UV radiation and trichostatin A in primary human keratinocytes.

Yao Shen, Wootae Ha, Wangyong Zeng, Dawn Queen, Liang Liu

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Trial
  2. Detection of germline variants in human population chronically exposed to high level natural background radiation in Kerala coast.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Tirbanibulin for Actinic Keratosis: Insights into the Mechanism of Action.Clinical, cosmetic and investigational dermatology · 2022
    Review
  10. Whole-Genome Sequencing IdentifiedFrontiers in medicine · 2022
    Article
  11. 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.

Yao ShenDepartment of Systems Biology, Columbia University, New York, New York, USA.
Wootae HaThe Hormel Institute, University of Minnesota, Austin, MN, USA.
Wangyong ZengDepartment of Dermatology, Columbia University, New York, USA.
Dawn QueenColumbia University Vagelos College of Physicians and Surgeons, New York, NY, 10032, USA.
Liang LiuThe Hormel Institute, University of Minnesota, Austin, MN, USA. LIU00965@umn.edu.

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Understanding the Biology of Chronic Ulcers: Histological and Molecular Basis...P30AR044535 · NIAMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BICKERS, DAVID RINSEY · 1997 to 2015
$6.9M
Epigenetic control of target gene activity by hairless in skin homeostasisK01AR064315 · NIAMS · UNIVERSITY OF MINNESOTA · PI LIU, LIANG · 2014 to 2018
$582k
NCI NIH HHS P30 CA013696NIAMS NIH HHS K01 AR064315NIAMS NIH HHS P30 AR044535
6 · The paper itself

Abstract

Canonical ultraviolet (UV) mutation type and spectra are traditionally defined by direct sequencing-based approaches to map mutations in a limited number of representative DNA elements. To obtain an unbiased view of genome wide UV mutation features, we performed whole exome-sequencing (WES) to profile single nucleotide substitutions in UVB-irradiated primary human keratinocytes. Cross comparison of UV mutation profiles under different UVB radiation conditions revealed that T > C transition was highly prevalent in addition to C > T transition. We also identified 5'-ACG-3' as a common sequence motif of C > T transition. Furthermore, our analyses uncovered several recurring UV mutations following acute UVB radiation affecting multiple genes including HRNR, TRIOBP, KCNJ12, and KMT2C, which are frequently mutated in skin cancers, indicating their potential role as founding mutations in UV-induced skin tumorigenesis. Pretreatment with trichostatin A, a pan-histone deacetylase inhibitor that renders chromatin decondensation, significantly decreased the number of mutations in UVB-irradiated keratinocytes. Unexpectedly, we found trichostatin A to be a mutagen that caused DNA damage and mutagenesis at least partly through increased reactive oxidation. In summary, our study reveals new UV mutation features following acute UVB radiation and identifies novel UV mutation hotspots that may potentially represent founding driver mutations in skin cancer development.

Indexed as

Exome SequencingMutationUltraviolet RaysComputational BiologyDNA DamageGenomic InstabilityHumansHydroxamic AcidsKeratinocytesPolymorphism, Single NucleotideProtein Synthesis InhibitorsHydroxamic AcidsProtein Synthesis Inhibitorstrichostatin A

Identifiers

PMID32188867
PMCPMC7080724

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.