The BCL-2 family member BOK promotes KRAS-driven lung cancer progression in a p53-dependent manner.
Journal
Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
received:
27
05
2021
accepted:
16
12
2021
revised:
01
12
2021
pubmed:
30
1
2022
medline:
11
3
2022
entrez:
29
1
2022
Statut:
ppublish
Résumé
A variety of cancer entities are driven by KRAS mutations, which remain difficult to target clinically. Survival pathways, such as resistance to cell death, may represent a promising treatment approach in KRAS mutated cancers. Based on the frequently observed genomic deletions of BCL-2-related ovarian killer (BOK) in cancer patients, we explored the function of BOK in a mutant Kras
Identifiants
pubmed: 35091677
doi: 10.1038/s41388-021-02161-1
pii: 10.1038/s41388-021-02161-1
pmc: PMC8881215
doi:
Substances chimiques
TP53 protein, human
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1376-1382Subventions
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 211179/Z/18/Z
Pays : United Kingdom
Informations de copyright
© 2021. The Author(s).
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