Drug resistance in glioblastoma: are persisters the key to therapy?
Drug resistance
chromatin remodeling
metabolism
persisters
tolerance
tumor environment
Journal
Cancer drug resistance (Alhambra, Calif.)
ISSN: 2578-532X
Titre abrégé: Cancer Drug Resist
Pays: United States
ID NLM: 101738710
Informations de publication
Date de publication:
2020
2020
Historique:
received:
28
04
2020
revised:
01
07
2020
accepted:
13
07
2020
entrez:
18
5
2022
pubmed:
7
8
2020
medline:
7
8
2020
Statut:
epublish
Résumé
Glioblastoma (GBM) represents the main form of brain tumors in adults, and one of the most aggressive cancers overall. The treatment of GBM is a combination of surgery (when possible), chemotherapy (usually Temozolomide, TMZ) and radiotherapy (RT). However, despite this heavy treatment, GBM invariably recur and the median length of survival following diagnosis is 12 to 15 months, with less than 10% of people surviving longer than five years. GBM is extremely resistant to most treatments because of its heterogeneous nature, which is associated with extreme clonal plasticity and the presence of cancer stem cells, refractory to TMZ- and RT-induced cell death. In this review, we explore the mechanisms by which cancer cells, and especially GBM, can acquire resistance to treatment. We describe and discuss the concept of persister/tolerant cells that precede and/or accompany the acquisition of resistance. Persister/tolerant cells are cancer cells that are not eliminated by treatment(s) because of different mechanisms ranging from dormancy/quiescence to senescence. We discuss the possibility of targeting these mechanisms in new therapeutic regimen.
Identifiants
pubmed: 35582442
doi: 10.20517/cdr.2020.29
pmc: PMC8992484
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
287-301Informations de copyright
© The Author(s) 2020.
Déclaration de conflit d'intérêts
All authors declared that there are no conflicts of interest.
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