ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2019
Recurrent Noncoding Mutations in Skin Cancers: UV Damage Susceptibility or Repair Inhibition as Primary Driver?
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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.
Who cites it
15 citing papers in PubMed.
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.Nucleic acids research · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Nature communications · 2026Article
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.bioRxiv : the preprint server for biology · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Research square · 2025Article
- Ultraviolet damage and repair maps inGenome research · 2025Article
- Genome-wide impact of cytosine methylation and DNA sequence context on UV-induced CPD formation.Environmental and molecular mutagenesis · 2024Article
- Detecting recurrent passenger mutations in melanoma by targeted UV damage sequencing.Nature communications · 2023Article
- Genome-wide maps of rare and atypical UV photoproducts reveal distinct patterns of damage formation and mutagenesis in yeast chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Widespread perturbation of ETS factor binding sites in cancer.Nature communications · 2023Article
- Molecular mechanism of UV damage modulation in nucleosomes.Computational and structural biotechnology journal · 2022Article
- CTCF binding modulates UV damage formation to promote mutation hot spots in melanoma.The EMBO journal · 2021Article
- Asymmetric repair of UV damage in nucleosomes imposes a DNA strand polarity on somatic mutations in skin cancer.Genome research · 2020Article
- Genomic sites hypersensitive to ultraviolet radiation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Deciphering the dynamic code: DNA recognition by transcription factors in the ever-changing genome.TranscriptionReview
- Super hotspots and super coldspots in the repair of UV-induced DNA damage in the human genome.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Somatic mutations arising in human skin cancers are heterogeneously distributed across the genome, meaning that certain genomic regions (e.g., heterochromatin or transcription factor binding sites) have much higher mutation densities than others. Regional variations in mutation rates are typically not a consequence of selection, as the vast majority of somatic mutations in skin cancers are passenger mutations that do not promote cell growth or transformation. Instead, variations in DNA repair activity, due to chromatin organization and transcription factor binding, have been proposed to be a primary driver of mutational heterogeneity in melanoma. However, as discussed in this review here, recent studies indicate that chromatin organization and transcription factor binding also significantly modulate the rate at which UV lesions form in DNA. The authors propose that local variations in lesion susceptibility may be an important driver of mutational hotspots in melanoma and other skin cancers, particularly at binding sites for ETS transcription factors.
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Registered trials
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.