TYMS promotes genomic instability and tumor progression in Ink4a/Arf null background.
Journal
Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562
Informations de publication
Date de publication:
06 2023
06 2023
Historique:
received:
29
06
2022
accepted:
14
04
2023
revised:
06
04
2023
medline:
8
6
2023
pubmed:
28
4
2023
entrez:
27
4
2023
Statut:
ppublish
Résumé
We previously showed that elevated TYMS exhibits oncogenic properties and promotes tumorigenesis after a long latency, suggesting cooperation with sequential somatic mutations. Here we report the cooperation of ectopic expression of human TYMS with loss of Ink4a/Arf, one of the most commonly mutated somatic events in human cancer. Using an hTS/Ink4a/Arf
Identifiants
pubmed: 37106126
doi: 10.1038/s41388-023-02694-7
pii: 10.1038/s41388-023-02694-7
pmc: PMC10244171
doi:
Substances chimiques
Cyclin-Dependent Kinase Inhibitor p16
0
Thymidylate Synthase
EC 2.1.1.45
Tumor Suppressor Protein p14ARF
0
TYMS protein, human
EC 2.1.1.45
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1926-1939Subventions
Organisme : NCI NIH HHS
ID : R01 CA188132
Pays : United States
Informations de copyright
© 2023. The Author(s).
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