% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Karajannis:126821,
author = {M. A. Karajannis and G. Legault and M. J. Fisher and S. S.
Milla and K. J. Cohen and J. H. Wisoff and D. H. Harter and
J. D. Goldberg and T. Hochman and A. Merkelson and M. C.
Bloom and A. J. Sievert and A. C. Resnick and G. Dhall and
D. Jones$^*$ and A. Korshunov$^*$ and S. Pfister$^*$ and C.
G. Eberhart and D. Zagzag and J. C. Allen},
title = {{P}hase {II} study of sorafenib in children with recurrent
or progressive low-grade astrocytomas.},
journal = {Neuro-Oncology},
volume = {16},
number = {10},
issn = {1523-5866},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {DKFZ-2017-02849},
pages = {1408 - 1416},
year = {2014},
abstract = {Activation of the RAS-RAF-MEK-ERK signaling pathway is
thought to be the key driver of pediatric low-grade
astrocytoma (PLGA) growth. Sorafenib is a multikinase
inhibitor targeting BRAF, VEGFR, PDGFR, and c-kit. This
multicenter phase II study was conducted to determine the
response rate to sorafenib in patients with recurrent or
progressive PLGA.Key eligibility criteria included age ≥ 2
years, progressive PLGA evaluable on MRI, and at least one
prior chemotherapy treatment. Sorafenib was administered
twice daily at 200 mg/m(2)/dose (maximum of 400 mg/dose) in
continuous 28-day cycles. MRI, including 3-dimensional
volumetric tumor analysis, was performed every 12 weeks.
BRAF molecular testing was performed on tumor tissue when
available.Eleven patients, including 3 with
neurofibromatosis type 1 (NF1), were evaluable for response;
5 tested positive for BRAF duplication. Nine patients
$(82\%)$ came off trial due to radiological tumor
progression after 2 or 3 cycles, including 3 patients with
confirmed BRAF duplication. Median time to progression was
2.8 months $(95\%$ CI, 2.1-31.0 months). Enrollment was
terminated early due to this rapid and unexpectedly high
progression rate. Tumor tissue obtained from 4 patients
after termination of the study showed viable pilocytic or
pilomyxoid astrocytoma.Sorafenib produced unexpected and
unprecedented acceleration of tumor growth in children with
PLGA, irrespective of NF1 or tumor BRAF status. In vitro
studies with sorafenib indicate that this effect is likely
related to paradoxical ERK activation. Close monitoring for
early tumor progression should be included in trials of
novel agents that modulate signal transduction.},
keywords = {Antineoplastic Agents (NLM Chemicals) / Phenylurea
Compounds (NLM Chemicals) / Protein Kinase Inhibitors (NLM
Chemicals) / Niacinamide (NLM Chemicals) / sorafenib (NLM
Chemicals)},
cin = {B062 / G380},
ddc = {610},
cid = {I:(DE-He78)B062-20160331 / I:(DE-He78)G380-20160331},
pnm = {312 - Functional and structural genomics (POF3-312)},
pid = {G:(DE-HGF)POF3-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:24803676},
pmc = {pmc:PMC4165419},
doi = {10.1093/neuonc/nou059},
url = {https://inrepo02.dkfz.de/record/126821},
}