Signaling levels mold the RAS mutation tropism of urethane.
RAS
cancer biology
carcinogenesis
codon bias
mouse
oncogenesis
protooncogenes
tumor initiation
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
17 05 2021
17 05 2021
Historique:
received:
03
02
2021
accepted:
01
04
2021
entrez:
17
5
2021
pubmed:
18
5
2021
medline:
27
10
2021
Statut:
epublish
Résumé
RAS genes are commonly mutated in human cancer. Despite many possible mutations, individual cancer types often have a 'tropism' towards a specific subset of RAS mutations. As driver mutations, these patterns ostensibly originate from normal cells. High oncogenic RAS activity causes oncogenic stress and different oncogenic mutations can impart different levels of activity, suggesting a relationship between oncoprotein activity and RAS mutation tropism. Here, we show that changing rare codons to common in the murine
Identifiants
pubmed: 33998997
doi: 10.7554/eLife.67172
pii: 67172
pmc: PMC8128437
doi:
pii:
Substances chimiques
Urethane
3IN71E75Z5
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : P01 CA203657
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA094184
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2021, Li and Counter.
Déclaration de conflit d'intérêts
SL, CC No competing interests declared
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