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@ARTICLE{John:164093,
author = {John, Peter and Waldt, Natalie and Liebich, Josephine and
Kesseler, Christoph and Schnabel, Stefan and Angenstein,
Frank and Sandalcioglu, I Erol and Scherlach, Cordula and
Sahm, Felix and Kirches, Elmar and Mawrin, Christian},
title = {{AKT}1{E}17{K} -mutated meningioma cell lines respond to
treatment with the {AKT} inhibitor {AZD}5363.},
journal = {Neuropathology $\&$ applied neurobiology},
volume = {48},
number = {2},
issn = {0305-1846},
address = {Oxford [u.a.]},
publisher = {Wiley-Blackwell},
reportid = {DZNE-2022-00756},
pages = {e12780},
year = {2022},
abstract = {Meningiomas are the most frequent primary brain tumours.
Recently, knowledge about the molecular drivers underlying
aggressive meningiomas has been expanded. A hotspot mutation
in the AKT1 gene (AKT1E17K ), which is found in meningiomas
at the convexity and especially at the skull base, has been
associated with earlier tumour recurrence.Here, we analysed
the effects of the AKT1E17K mutation and treatment response
to the Akt inhibitor AZD5363 in transgenic meningioma cell
clones and mouse xenografts modelling convexity or skull
base meningiomas.We show that the AKTE17K mutation
significantly enhances meningioma cell proliferation and
colony size in vitro, resulting in significantly shortened
survival times of mice carrying convexity or skull base
AKT1E17K xenografts. Treatment of mutant cells or xenografts
(150 mg/kg/d) with AZD5363 revealed a significant decrease
in cell proliferation and colony size and a prolongation of
mouse survival. Western blots revealed activation of AKT1
kinase (phosphorylation at Ser273 and Thr308) by the E17K
mutation in human meningioma samples and in our in vitro and
in vivo models.Our data suggest that AKT1E17K mutated
meningiomas are a promising selective target for AZD5363.},
keywords = {Animals / Cell Line, Tumor / Cell Proliferation: drug
effects / Enzyme Inhibitors: pharmacology / Humans /
Meningeal Neoplasms: genetics / Meningeal Neoplasms:
pathology / Meningioma: genetics / Meningioma: pathology /
Mice / Proto-Oncogene Proteins c-akt: antagonists $\&$
inhibitors / Proto-Oncogene Proteins c-akt: genetics /
Pyrimidines: pharmacology / Pyrroles: pharmacology / Skull
Base Neoplasms: genetics / Skull Base Neoplasms: pathology /
AKT1 (Other) / meningioma (Other) / targeted therapy (Other)
/ Enzyme Inhibitors (NLM Chemicals) / Pyrimidines (NLM
Chemicals) / Pyrroles (NLM Chemicals) / Proto-Oncogene
Proteins c-akt (NLM Chemicals) / capivasertib (NLM
Chemicals)},
cin = {AG Angenstein},
ddc = {610},
cid = {I:(DE-2719)1310004},
pnm = {351 - Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34837233},
doi = {10.1111/nan.12780},
url = {https://pub.dzne.de/record/164093},
}