Histomolecular characterization of intracranial meningiomas developed in patients exposed to high-dose cyproterone acetate: an antiandrogen treatment.
AKT1
PIK3CA
cyproterone acetate
meningioma
molecular pathology
Journal
Neuro-oncology advances
ISSN: 2632-2498
Titre abrégé: Neurooncol Adv
Pays: England
ID NLM: 101755003
Informations de publication
Date de publication:
Historique:
entrez:
10
7
2020
pubmed:
28
5
2019
medline:
28
5
2019
Statut:
epublish
Résumé
Meningiomas are the most common primary intracranial tumors in adults. The relationship between meningiomas and exogenous sex hormones such as cyproterone acetate (CPA) is well documented, yet the underlying mechanisms remain unknown. Defining the histomolecular status of meningiomas developed on CPA would help us to better understand the oncogenesis of these tumors. We identified 30 patients operated for a meningioma after long-term high-dose CPA therapy and with a history of CPA discontinuation before establishing the indication for surgical intervention. We used array-comparative genomic hybridization (to characterize copy number changes in those 30 meningiomas and subsequently performed next-generation sequencing with the National Institute of Cancer (INCa) solid tumor panel, which is a targeted panel of clinically actionable genes. We also examined grade, type, and clinical features. We identified Our study shows that low-grade meningothelial meningiomas of the skull base are predominant in CPA meningiomas. We identified PIK3CA/AKT1 pathway as a hypothetical actor in onco-pharmacological interaction between meningiomas and CPA. This signaling pathway could be an interesting target for precision medicine trials in meningioma patients who have been subjected to CPA. Our results could invite the scientific community to review the current classification of meningiomas and to evolve toward more specific histomolecular classification.
Sections du résumé
BACKGROUND
BACKGROUND
Meningiomas are the most common primary intracranial tumors in adults. The relationship between meningiomas and exogenous sex hormones such as cyproterone acetate (CPA) is well documented, yet the underlying mechanisms remain unknown. Defining the histomolecular status of meningiomas developed on CPA would help us to better understand the oncogenesis of these tumors.
METHODS
METHODS
We identified 30 patients operated for a meningioma after long-term high-dose CPA therapy and with a history of CPA discontinuation before establishing the indication for surgical intervention. We used array-comparative genomic hybridization (to characterize copy number changes in those 30 meningiomas and subsequently performed next-generation sequencing with the National Institute of Cancer (INCa) solid tumor panel, which is a targeted panel of clinically actionable genes. We also examined grade, type, and clinical features.
RESULTS
RESULTS
We identified
CONCLUSION
CONCLUSIONS
Our study shows that low-grade meningothelial meningiomas of the skull base are predominant in CPA meningiomas. We identified PIK3CA/AKT1 pathway as a hypothetical actor in onco-pharmacological interaction between meningiomas and CPA. This signaling pathway could be an interesting target for precision medicine trials in meningioma patients who have been subjected to CPA. Our results could invite the scientific community to review the current classification of meningiomas and to evolve toward more specific histomolecular classification.
Identifiants
pubmed: 32642646
doi: 10.1093/noajnl/vdz003
pii: vdz003
pmc: PMC7212922
doi:
Types de publication
Journal Article
Langues
eng
Pagination
vdz003Informations de copyright
© The Author(s) 2019. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.
Références
J Surg Oncol. 1986 Mar;31(3):182-3
pubmed: 3724170
J Neurol Neurosurg Psychiatry. 1958 May;21(2):89-91
pubmed: 13539648
Gynecol Oncol. 2014 Nov;135(2):312-7
pubmed: 25172762
Acta Neurochir (Wien). 1986;79(1):42-7
pubmed: 3953323
Acta Neurochir (Wien). 2017 Mar;159(3):403-418
pubmed: 28093610
Neuro Oncol. 2016 Feb;18(2):269-74
pubmed: 26323607
Virchows Arch. 2014 Oct;465(4):473-85
pubmed: 25146167
J Mol Diagn. 2017 Jan;19(1):4-23
pubmed: 27993330
Neurochirurgie. 2018 Mar;64(1):22-28
pubmed: 25245924
J Neurosurg. 2006 Jul;105(1):60-4
pubmed: 16871881
Acta Neuropathol. 2016 Jun;131(6):803-20
pubmed: 27157931
Pathologica. 2009 Jun;101(3):115-8
pubmed: 19886545
Neuro Oncol. 2016 May;18(5):603-4
pubmed: 27257280
Br J Clin Pharmacol. 2011 Dec;72(6):965-8
pubmed: 21627676
Acta Neurochir (Wien). 2010 Nov;152(11):1955-6
pubmed: 20811919
Ann Oncol. 2018 Mar 1;29(3):681-686
pubmed: 29206892
Acta Neurochir (Wien). 2015 Oct;157(10):1741-6
pubmed: 26264069
Arch Pathol Lab Med. 1983 Feb;107(2):75-80
pubmed: 6687423
Int J Cancer. 2008 Mar 1;122(5):1189-94
pubmed: 17990317
Neurosurgery. 1996 Jul;39(1):2-7; discussion 8-9
pubmed: 8805134
Oncotarget. 2015 May 10;6(13):10671-88
pubmed: 25965831
Neuro Oncol. 2017 Aug 1;19(8):1088-1096
pubmed: 28482067
J Neurosci Res. 2016 Dec;94(12):1604-1612
pubmed: 27376782
Oncogene. 2008 Sep 18;27(41):5497-510
pubmed: 18794884
Neurosurgery. 2005 Dec;57(6):1088-95; discussion 1088-95
pubmed: 16331155
Science. 2013 Mar 1;339(6123):1077-80
pubmed: 23348505
J Neuropathol Exp Neurol. 1986 Sep;45(5):588-608
pubmed: 3746345
Acta Neuropathol. 2007 Aug;114(2):97-109
pubmed: 17618441
J Neurooncol. 2010 Sep;99(3):379-91
pubmed: 20809251
J Natl Cancer Inst. 2017 Mar 1;109(3):1-4
pubmed: 28376212
J Neurosurg. 2010 May;112(5):920-4
pubmed: 19731987
J Craniomaxillofac Surg. 2005 Aug;33(4):260-6
pubmed: 15978821
J Clin Pathol. 2004 Oct;57(10):1033-7
pubmed: 15452155
Biomed Res Int. 2015;2015:267831
pubmed: 26146614
Neuro Oncol. 2016 May;18(5):649-55
pubmed: 26826201
Oncotarget. 2017 Mar 7;8(10):17070-17080
pubmed: 28177878
Br J Cancer. 2006 Feb 27;94(4):455-9
pubmed: 16449998
PLoS One. 2015 Oct 15;10(10):e0140479
pubmed: 26469692
J Neurooncol. 2007 May;82(3):319-21
pubmed: 17177106
Front Surg. 2016 Jul 06;3:40
pubmed: 27458586