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@ARTICLE{Zheng:168443,
author = {T. Zheng$^*$ and D. R. Ghasemi$^*$ and K. Okonechnikov$^*$
and A. Korshunov$^*$ and M. Sill$^*$ and K. K. Maass$^*$ and
P. Benites Goncalves da Silva$^*$ and M. Ryzhova$^*$ and J.
Gojo$^*$ and D. Stichel$^*$ and A. Arabzade and R. Kupp and
J. Benzel$^*$ and S. Taya and T. Adachi and R. Shiraishi and
N. U. Gerber and D. Sturm$^*$ and J. Ecker$^*$ and P.
Sievers$^*$ and F. Selt and R. Chapman and C. Haberler and
D. Figarella-Branger and G. Reifenberger$^*$ and G.
Fleischhack and S. Rutkowski and A. M. Donson and V.
Ramaswamy and D. Capper$^*$ and D. W. Ellison and C. C.
Herold-Mende and U. Schuller and S. Brandner and P. Hernaiz
Driever and J. M. Kros and M. Snuderl and T. Milde$^*$ and
R. G. Grundy and M. Hoshino and S. C. Mack and R. J.
Gilbertson and D. T. W. Jones$^*$ and M. Kool$^*$ and A. von
Deimling$^*$ and S. M. Pfister$^*$ and F. Sahm$^*$ and D.
Kawauchi$^*$ and K. Pajtler$^*$},
title = {{C}ross-species genomics reveals oncogenic dependencies in
{ZFTA}/{C}11orf95 fusion-positive supratentorial
ependymomas.},
journal = {Cancer discovery},
volume = {11},
number = {9},
issn = {2159-8290},
address = {Philadelphia, Pa.},
reportid = {DKFZ-2021-00917},
pages = {2230-2247},
year = {2021},
note = {#EA:B062#LA:B062#B300# /2021 Sep;11(9):2230-2247},
abstract = {Molecular groups of supratentorial ependymomas comprise
tumors with ZFTA-RELA or YAP1-involving fusions and
fusion-negative subependymoma. However, occasionally
supratentorial ependymomas cannot be readily assigned to any
of these groups due to lack of detection of a typical fusion
and/or ambiguous DNA methylation-based classification. An
unbiased approach with a cohort of unprecedented size
revealed distinct methylation clusters composed of tumors
with ependymal but also various other histological features
containing alternative translocations that shared ZFTA as a
partner gene. Somatic overexpression of ZFTA-associated
fusion genes in the developing cerebral cortex is capable of
inducing tumor formation in vivo, and cross-species
comparative analyses identified GLI2 as a key downstream
regulator of tumorigenesis in all tumors. Targeting GLI2
with arsenic trioxide caused extended survival of
tumor-bearing animals, indicating a potential therapeutic
vulnerability in ZFTA fusion-positive tumors.},
cin = {B062 / HD01 / B300 / B360 / B310 / ED01 / BE01},
ddc = {610},
cid = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331 /
I:(DE-He78)B300-20160331 / I:(DE-He78)B360-20160331 /
I:(DE-He78)B310-20160331 / I:(DE-He78)ED01-20160331 /
I:(DE-He78)BE01-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33879448},
doi = {10.1158/2159-8290.CD-20-0963},
url = {https://inrepo02.dkfz.de/record/168443},
}