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@ARTICLE{Selt:124405,
author = {F. Selt$^*$ and J. Hohloch$^*$ and T. Hielscher$^*$ and F.
Sahm$^*$ and D. Capper$^*$ and A. Korshunov$^*$ and D.
Usta$^*$ and S. Brabetz$^*$ and J. Ridinger$^*$ and J.
Ecker$^*$ and I. Oehme$^*$ and J. Gronych$^*$ and V.
Marquardt$^*$ and D. Pauck$^*$ and H. Bächli and C. D.
Stiles and A. von Deimling$^*$ and M. Remke$^*$ and M. U.
Schuhmann and S. Pfister$^*$ and T. Brummer and D. Jones$^*$
and O. Witt$^*$ and T. Milde$^*$},
title = {{E}stablishment and application of a novel patient-derived
{KIAA}1549:{BRAF}-driven pediatric pilocytic astrocytoma
model for preclinical drug testing.},
journal = {OncoTarget},
volume = {8},
number = {7},
issn = {1949-2553},
address = {[S.l.]},
publisher = {Impact Journals LLC},
reportid = {DKFZ-2017-01284},
pages = {11460-11479},
year = {2017},
abstract = {Pilocytic astrocytoma (PA) is the most frequent pediatric
brain tumor. Activation of the MAPK pathway is well
established as the oncogenic driver of the disease. It is
most frequently caused by KIAA1549:BRAF fusions, and leads
to oncogene induced senescence (OIS). OIS is thought to be a
major reason for growth arrest of PA cells in vitro and in
vivo, preventing establishment of PA cultures. Hence, valid
preclinical models are currently very limited, but
preclinical testing of new compounds is urgently needed. We
transduced the PA short-term culture DKFZ-BT66 derived from
the PA of a 2-year old patient with a doxycycline-inducible
system coding for Simian Vacuolating Virus 40 Large T
Antigen (SV40-TAg). SV40-TAg inhibits TP53/CDKN1A and
CDKN2A/RB1, two pathways critical for OIS induction and
maintenance. DNA methylation array and KIAA1549:BRAF fusion
analysis confirmed pilocytic astrocytoma identity of
DKFZ-BT66 cells after establishment. Readouts were analyzed
in proliferating as well as senescent states, including cell
counts, viability, cell cycle analysis, expression of
SV40-Tag, CDKN2A (p16), CDKN1A (p21), and TP53 (p53)
protein, and gene-expression profiling. Selected MAPK
inhibitors (MAPKi) including clinically available MEK
inhibitors (MEKi) were tested in vitro. Expression of
SV40-TAg enabled the cells to bypass OIS and to resume
proliferation with a mean doubling time of 45h allowing for
propagation and long-term culture. Withdrawal of doxycycline
led to an immediate decrease of SV40-TAg expression,
appearance of senescent morphology, upregulation of CDKI
proteins and a subsequent G1 growth arrest in line with the
re-induction of senescence. DKFZ-BT66 cells still underwent
replicative senescence that was overcome by TERT expression.
Testing of a set of MAPKi revealed differential responses in
DKFZ-BT66. MEKi efficiently inhibited MAPK signaling at
clinically achievable concentrations, while BRAF V600E- and
RAF Type II inhibitors showed paradoxical activation. Taken
together, we have established the first patient-derived long
term expandable PA cell line expressing the
KIAA1549:BRAF-fusion suitable for preclinical drug testing.},
cin = {G340 / C060 / G380 / B062 / B060 / L401 / L101 / L601},
ddc = {610},
cid = {I:(DE-He78)G340-20160331 / I:(DE-He78)C060-20160331 /
I:(DE-He78)G380-20160331 / I:(DE-He78)B062-20160331 /
I:(DE-He78)B060-20160331 / I:(DE-He78)L401-20160331 /
I:(DE-He78)L101-20160331 / I:(DE-He78)L601-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28002790},
pmc = {pmc:PMC5355278},
doi = {10.18632/oncotarget.14004},
url = {https://inrepo02.dkfz.de/record/124405},
}