ArticleNature communications2023
Detecting recurrent passenger mutations in melanoma by targeted UV damage sequencing.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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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.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- 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
- Light-based footprinting of a eukaryotic genome.Science advances · 2026Article
- Genome-wide mutation spectra of canonical and atypical UV photoproducts in S. cerevisiae.Nucleic acids research · 2026Article
- Altered benzo[a]pyrene adduct formation in nucleosomes establishes distinct mutational patterns in lung cancer.The Journal of biological chemistry · 2026Article
- Mechanisms of the Antiproliferative Effects of SIRT6 Inhibition in Melanoma: A Multi-Omics Analysis.Cancers · 2026Article
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.bioRxiv : the preprint server for biology · 2026Article
- Classification of driver and passenger mutations in different cancer types using deep neural networks.Bioinformatics advances · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Research square · 2025Article
- Mapping transcription factor binding sites by learning UV damage fingerprints.Nucleic acids research · 2025Article
- From Transcription Factors Dysregulation to Malignancy: In Silico Reconstruction of Cancer's Foundational Drivers-The Eternity Triangle.International journal of molecular sciences · 2025Article
- Reannotation of cancer mutations based on expressed RNA transcripts reveals functional non-coding mutations in melanoma.American journal of human genetics · 2025Article
- Ultraviolet damage and repair maps inGenome research · 2025Article
- The epigenetic landscape shapes smoking-induced mutagenesis by modulating DNA damage susceptibility and repair efficiency.Nucleic acids research · 2025Article
- SpecificbioRxiv : the preprint server for biology · 2024Article
- Methods and applications of genome-wide profiling of DNA damage and rare mutations.Nature reviews. Genetics · 2024Review
- Mechanistic basis of atypical TERT promoter mutations.Nature communications · 2024Article
- Ultraviolet (UV) radiation: a double-edged sword in cancer development and therapy.Molecular biomedicine · 2024Review
- Prognostic and therapeutic roles ofAging · 2024Article
- High UV damage and low repair, but not cytosine deamination, stimulate mutation hotspots at ETS binding sites in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Sequencing of melanomas has identified hundreds of recurrent mutations in both coding and non-coding DNA. These include a number of well-characterized oncogenic driver mutations, such as coding mutations in the BRAF and NRAS oncogenes, and non-coding mutations in the promoter of telomerase reverse transcriptase (TERT). However, the molecular etiology and significance of most of these mutations is unknown. Here, we use a new method known as CPD-capture-seq to map UV-induced cyclobutane pyrimidine dimers (CPDs) with high sequencing depth and single nucleotide resolution at sites of recurrent mutations in melanoma. Our data reveal that many previously identified drivers and other recurrent mutations in melanoma occur at CPD hotspots in UV-irradiated melanocytes, often associated with an overlapping binding site of an E26 transformation-specific (ETS) transcription factor. In contrast, recurrent mutations in the promoters of a number of known or suspected cancer genes are not associated with elevated CPD levels. Our data indicate that a subset of recurrent protein-coding mutations are also likely caused by ETS-induced CPD hotspots. This analysis indicates that ETS proteins profoundly shape the mutation landscape of melanoma and reveals a method for distinguishing potential driver mutations from passenger mutations whose recurrence is due to elevated UV damage.
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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.