Journal Article

FZJ-2018-02231

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Dabrafenib Treatment in a Patient with an Epithelioid Glioblastoma and BRAF V600E Mutation

Ceccon, G. ; Werner, J.-M. ; Dunkl, V. ; Tscherpel, C.FZJ* ; Stoffels, G.FZJ* ; Brunn, A. ; Deckert, M. ; Fink, G. R.FZJ* ; Galldiks, N. (Corresponding author)FZJ*

2018
Molecular Diversity Preservation International Basel

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Please use a persistent id in citations: http://hdl.handle.net/2128/17954  doi:10.3390/ijms19041090

Abstract: Novel therapeutic targets in malignant glioma patients are urgently needed. Point mutations of the v-Raf murine sarcoma viral oncogene homolog B (BRAF) gene occur predominantly in melanoma patients, but may also occur in gliomas. Thus, this is a target of great interest for this group of patients. In a nine-year-old male patient, an anaplastic astrocytoma in the left temporoparietal region was diagnosed histologically. After first- and second-line treatment, a malignant progression to a secondary glioblastoma was observed ten years after the initial diagnosis. Within the following seven years, all other conventional treatment options were exhausted. At this time point, recurrent tumor histology revealed an epithelioid glioblastoma, without a mutation in the isocitrate dehydrogenase gene (IDH wild-type). In order to identify a potential target for an experimental salvage therapy, mutational tumor analysis showed a BRAF V600E mutation. Consecutively, dabrafenib treatment was initiated. The patient remained clinically stable, and follow-up magnetic resonance images (MRI) were consistent with “Stable Disease” according to the Response Assessment in Neuro-Oncology Working Group (RANO) criteria for the following ten months until tumor progression was detected. The patient died 16 months after dabrafenib treatment initiation. Particularly in younger glioma patients as well as in patients with an epithelioid glioblastoma, screening for a V600E BRAF mutation is promising since, in these cases, targeted therapy with BRAF inhibitors seems to be a useful salvage treatment option.

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Contributing Institute(s):

1. Kognitive Neurowissenschaften (INM-3)
2. Physik der Medizinischen Bildgebung (INM-4)

Research Program(s):

1. 572 - (Dys-)function and Plasticity (POF3-572) (POF3-572)

Appears in the scientific report 2018

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Database coverage:
; ; ; ; Current Contents - Physical, Chemical and Earth Sciences ; DOAJ Seal ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection

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