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@ARTICLE{Thomas:168126,
author = {C. Thomas and F. Thierfelder$^*$ and M. Träger and P.
Soschinski and M. Müther and D. Edelmann$^*$ and A.
Förster and C. Geiler and H.-Y. Kim$^*$ and K. Filipski$^*$
and P. Harter$^*$ and J. Schittenhelm and F. Eckert and G.
Ntoulias and S.-A. May and W. Stummer and J. Onken and P.
Vajkoczy and U. Schüller and F. L. Heppner$^*$ and D.
Capper$^*$ and A. Koch$^*$ and D. Kaul and W. Paulus and M.
Hasselblatt and L. Schweizer$^*$},
title = {{TERT} promoter mutation and chromosome 6 loss define a
high-risk subtype of ependymoma evolving from posterior
fossa subependymoma.},
journal = {Acta neuropathologica},
volume = {141},
number = {6},
issn = {1432-0533},
address = {Heidelberg},
publisher = {Springer},
reportid = {DKFZ-2021-00694},
pages = {959-970},
year = {2021},
note = {141(6):959-970},
abstract = {Subependymomas are benign tumors characteristically
encountered in the posterior fossa of adults that show
distinct epigenetic profiles assigned to the molecular group
'subependymoma, posterior fossa' (PFSE) of the recently
established DNA methylation-based classification of central
nervous system tumors. In contrast, most posterior fossa
ependymomas exhibit a more aggressive biological behavior
and are allocated to the molecular subgroups PFA or PFB. A
subset of ependymomas shows epigenetic similarities with
subependymomas, but the precise biology of these tumors and
their potential relationships remain unknown. We therefore
set out to characterize epigenetic traits, mutational
profiles, and clinical outcomes of 50 posterior fossa
ependymal tumors of the PFSE group. On histo-morphology,
these tumors comprised 12 ependymomas, 14 subependymomas and
24 tumors with mixed ependymoma-subependymoma morphology.
Mixed ependymoma-subependymoma tumors varied in their extent
of ependymoma differentiation $(2-95\%)$ but consistently
exhibited global epigenetic profiles of the PFSE group.
Selective methylome analysis of microdissected tumor
components revealed CpG signatures in mixed tumors that
coalesce with their pure counterparts. Loss of chr6 (20/50
cases), as well as TERT mutations (21/50 cases), were
frequent events enriched in tumors with pure ependymoma
morphology (p < 0.001) and confined to areas with ependymoma
differentiation in mixed tumors. Clinically, pure ependymoma
phenotype, chr6 loss, and TERT mutations were associated
with shorter progression-free survival (each p < 0.001). In
conclusion, our results suggest that subependymomas may
acquire genetic and epigenetic changes throughout tumor
evolution giving rise to subclones with ependymoma
morphology (resulting in mixed tumors) that eventually
overpopulate the subependymoma component (pure PFSE
ependymomas).},
keywords = {Chromosome 6 (Other) / DNA methylation (Other) / Mixed
ependymoma–subependymoma (Other) / Subependymoma (Other) /
TERT (Other)},
cin = {BE01 / FM01 / C060},
ddc = {610},
cid = {I:(DE-He78)BE01-20160331 / I:(DE-He78)FM01-20160331 /
I:(DE-He78)C060-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33755803},
doi = {10.1007/s00401-021-02300-8},
url = {https://inrepo02.dkfz.de/record/168126},
}