Mutational processes of tobacco smoking and APOBEC activity generate protein-truncating mutations in cancer genomes.
Journal
Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440
Informations de publication
Date de publication:
03 11 2023
03 11 2023
Historique:
medline:
6
11
2023
pubmed:
3
11
2023
entrez:
3
11
2023
Statut:
ppublish
Résumé
Mutational signatures represent a genomic footprint of endogenous and exogenous mutational processes through tumor evolution. However, their functional impact on the proteome remains incompletely understood. We analyzed the protein-coding impact of single-base substitution (SBS) signatures in 12,341 cancer genomes from 18 cancer types. Stop-gain mutations (SGMs) (i.e., nonsense mutations) were strongly enriched in SBS signatures of tobacco smoking, APOBEC cytidine deaminases, and reactive oxygen species. These mutational processes alter specific trinucleotide contexts and thereby substitute serines and glutamic acids with stop codons. SGMs frequently affect cancer hallmark pathways and tumor suppressors such as
Identifiants
pubmed: 37922356
doi: 10.1126/sciadv.adh3083
pmc: PMC10624356
doi:
Substances chimiques
APOBEC3A protein, human
EC 3.5.4.5
Cytidine Deaminase
EC 3.5.4.5
APOBEC Deaminases
EC 3.5.4.5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
eadh3083Références
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