Changing paradigms in oncology: Toward noncytotoxic treatments for advanced gliomas.
cancer epigenetics
epigenetic
glioma
glioma therapy
neurooncology
Journal
International journal of cancer
ISSN: 1097-0215
Titre abrégé: Int J Cancer
Pays: United States
ID NLM: 0042124
Informations de publication
Date de publication:
01 11 2022
01 11 2022
Historique:
revised:
12
05
2022
received:
23
02
2022
accepted:
13
05
2022
pubmed:
24
5
2022
medline:
15
9
2022
entrez:
23
5
2022
Statut:
ppublish
Résumé
Glial-lineage malignancies (gliomas) recurrently mutate and/or delete the master regulators of apoptosis p53 and/or p16/CDKN2A, undermining apoptosis-intending (cytotoxic) treatments. By contrast to disrupted p53/p16, glioma cells are live-wired with the master transcription factor circuits that specify and drive glial lineage fates: these transcription factors activate early-glial and replication programs as expected, but fail in their other usual function of forcing onward glial lineage-maturation-late-glial genes have constitutively "closed" chromatin requiring chromatin-remodeling for activation-glioma-genesis disrupts several epigenetic components needed to perform this work, and simultaneously amplifies repressing epigenetic machinery instead. Pharmacologic inhibition of repressing epigenetic enzymes thus allows activation of late-glial genes and terminates glioma self-replication (self-replication = replication without lineage-maturation), independent of p53/p16/apoptosis. Lineage-specifying master transcription factors therefore contrast with p53/p16 in being enriched in self-replicating glioma cells, reveal a cause-effect relationship between aberrant epigenetic repression of late-lineage programs and malignant self-replication, and point to specific epigenetic targets for noncytotoxic glioma-therapy.
Identifiants
pubmed: 35603902
doi: 10.1002/ijc.34131
pmc: PMC9474618
mid: NIHMS1810009
doi:
Substances chimiques
Chromatin
0
Cyclin-Dependent Kinase Inhibitor p16
0
Transcription Factors
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1431-1446Subventions
Organisme : NCI NIH HHS
ID : R01 CA138858
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA204373
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA263430
Pays : United States
Organisme : NHLBI NIH HHS
ID : R44 HL135896
Pays : United States
Informations de copyright
© 2022 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.
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