Targeting tumor phenotypic plasticity and metabolic remodeling in adaptive cross-drug tolerance.
Antineoplastic Agents
/ pharmacology
Drug Delivery Systems
Enzyme Inhibitors
/ pharmacology
Glucose
/ metabolism
Glucosephosphate Dehydrogenase
/ antagonists & inhibitors
Humans
MCF-7 Cells
Neoplasm Metastasis
Neoplasm Proteins
/ antagonists & inhibitors
Neoplasms
/ drug therapy
Pentose Phosphate Pathway
/ drug effects
Journal
Science signaling
ISSN: 1937-9145
Titre abrégé: Sci Signal
Pays: United States
ID NLM: 101465400
Informations de publication
Date de publication:
20 08 2019
20 08 2019
Historique:
entrez:
22
8
2019
pubmed:
23
8
2019
medline:
14
8
2020
Statut:
epublish
Résumé
Metastable phenotypic state transitions in cancer cells can lead to the development of transient adaptive resistance or tolerance to chemotherapy. Here, we report that the acquisition of a phenotype marked by increased abundance of CD44 (CD44
Identifiants
pubmed: 31431543
pii: 12/595/eaas8779
doi: 10.1126/scisignal.aas8779
pmc: PMC7261372
mid: NIHMS1579586
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Enzyme Inhibitors
0
Neoplasm Proteins
0
Glucosephosphate Dehydrogenase
EC 1.1.1.49
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : U01 CA214411
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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