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@ARTICLE{Kessler:132534,
author = {T. Kessler$^*$ and F. Sahm$^*$ and A. Sadik$^*$ and D.
Stichel$^*$ and A. Hertenstein$^*$ and G. Reifenberger and
A. Zacher and M. Sabel and G. Tabatabai$^*$ and J.
Steinbach$^*$ and U. Sure$^*$ and D. Krex$^*$ and A.-L.
Grosu$^*$ and M. Bewerunge-Hudler$^*$ and D. Jones$^*$ and
S. Pfister$^*$ and M. Weller and C. Opitz$^*$ and M.
Bendszus and A. von Deimling$^*$ and M. Platten$^*$ and W.
Wick$^*$},
title = {{M}olecular differences in {IDH} wildtype glioblastoma
according to {MGMT} promoter methylation.},
journal = {Neuro-Oncology},
volume = {20},
number = {3},
issn = {1523-5866},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {DKFZ-2018-00218},
pages = {367 - 379},
year = {2018},
abstract = {O6-methylguanine-DNA-methyltransferase (MGMT) promoter
methylation status is a predictive biomarker in
glioblastoma. We investigated whether this marker
furthermore defines a molecularly distinct tumor subtype
with clinically different outcome.We analyzed copy number
variation (CNV) and methylation profiles of 1095 primary and
92 progressive isocitrate dehydrogenase wildtype
glioblastomas, including paired samples from 49 patients.
DNA mutation data from 182 glioblastoma samples of The
Cancer Genome Atlas (TCGA) and RNA expression from 107 TCGA
and 55 Chinese Glioma Genome Atlas samples were
analyzed.Among untreated glioblastomas, MGMT promoter
methylated (mMGMT) and unmethylated (uMGMT) tumors did not
show different CNV or specific gene mutations, but a higher
mutation count in mMGMT tumors. We identified 3 methylation
clusters. Cluster 1 showed the highest average methylation
and was enriched for mMGMT tumors. Seventeen genes including
gastrulation brain homeobox 2 (GBX2) were found to be
hypermethylated and downregulated on the mRNA level in mMGMT
tumors. In progressive glioblastomas, platelet derived
growth factor receptor alpha (PDGFRA) and GLI2
amplifications were enriched in mMGMT tumors. Methylated
MGMT tumors gain PDGFRA amplification of PDGFRA, whereas
uMGMT tumors with amplified PDGFRA frequently lose this
amplification upon progression. Glioblastoma patients
surviving <6 months and with mMGMT harbored less frequent
epidermal growth factor receptor (EGFR) amplifications, more
frequent TP53 mutations, and a higher tumor necrosis
factor-nuclear factor-kappaB (TNF-NFκB) pathway activation
compared with patients surviving >12 months.MGMT promoter
methylation status does not define a molecularly distinct
glioblastoma subpopulation among untreated tumors.
Progressive mMGMT glioblastomas and mMGMT tumors of patients
with short survival tend to have more unfavorable molecular
profiles.},
cin = {G370 / L101 / G380 / G161 / L801 / L601 / W110 / G160 /
B062},
ddc = {610},
cid = {I:(DE-He78)G370-20160331 / I:(DE-He78)L101-20160331 /
I:(DE-He78)G380-20160331 / I:(DE-He78)G161-20160331 /
I:(DE-He78)L801-20160331 / I:(DE-He78)L601-20160331 /
I:(DE-He78)W110-20160331 / I:(DE-He78)G160-20160331 /
I:(DE-He78)B062-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29016808},
pmc = {pmc:PMC5817966},
doi = {10.1093/neuonc/nox160},
url = {https://inrepo02.dkfz.de/record/132534},
}