Radiation-induced gliomas represent H3-/IDH-wild type pediatric gliomas with recurrent PDGFRA amplification and loss of CDKN2A/B.
Adolescent
Adult
Child
Chromosome Deletion
Cluster Analysis
Cyclin-Dependent Kinase Inhibitor p15
/ metabolism
Cyclin-Dependent Kinase Inhibitor p16
/ metabolism
DNA Methylation
/ genetics
Female
Gene Amplification
Gene Expression Regulation, Neoplastic
Gene Rearrangement
/ genetics
Genome, Human
Glioma
/ genetics
Humans
Kaplan-Meier Estimate
Male
Middle Aged
Neoplasm Recurrence, Local
/ pathology
Radiation
Receptor, Platelet-Derived Growth Factor alpha
/ genetics
Transcription, Genetic
Young Adult
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
20 09 2021
20 09 2021
Historique:
received:
22
05
2020
accepted:
12
08
2021
entrez:
21
9
2021
pubmed:
22
9
2021
medline:
13
10
2021
Statut:
epublish
Résumé
Long-term complications such as radiation-induced second malignancies occur in a subset of patients following radiation-therapy, particularly relevant in pediatric patients due to the long follow-up period in case of survival. Radiation-induced gliomas (RIGs) have been reported in patients after treatment with cranial irradiation for various primary malignancies such as acute lymphoblastic leukemia (ALL) and medulloblastoma (MB). We perform comprehensive (epi-) genetic and expression profiling of RIGs arising after cranial irradiation for MB (n = 23) and ALL (n = 9). Our study reveals a unifying molecular signature for the majority of RIGs, with recurrent PDGFRA amplification and loss of CDKN2A/B and an absence of somatic hotspot mutations in genes encoding histone 3 variants or IDH1/2, uncovering diagnostic markers and potentially actionable targets.
Identifiants
pubmed: 34545083
doi: 10.1038/s41467-021-25708-y
pii: 10.1038/s41467-021-25708-y
pmc: PMC8452680
doi:
Substances chimiques
CDKN2A protein, human
0
CDKN2B protein, human
0
Cyclin-Dependent Kinase Inhibitor p15
0
Cyclin-Dependent Kinase Inhibitor p16
0
Receptor, Platelet-Derived Growth Factor alpha
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5530Informations de copyright
© 2021. The Author(s).
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