H3K27me3 loss indicates an increased risk of recurrence in the Tübingen meningioma cohort.
H3K27
H3K27me3
histone methylation
meningioma
recurrence-free survival
Journal
Neuro-oncology
ISSN: 1523-5866
Titre abrégé: Neuro Oncol
Pays: England
ID NLM: 100887420
Informations de publication
Date de publication:
02 08 2021
02 08 2021
Historique:
pubmed:
29
12
2020
medline:
7
8
2021
entrez:
28
12
2020
Statut:
ppublish
Résumé
A loss of the trimethylation of lysine 27 of histone H3 (H3K27me3) in meningioma has been recently suggested as an adjunct to identify subsets of higher risk of recurrence. The aim of the present study was to assess the prognostic value of H3K27 histone trimethylation and its potential clinical utility in the "Tübingen meningioma cohort." Patients who underwent meningioma resection between October 2003 and December 2015 at the University Hospital Tübingen were included. Immunohistochemical stainings for H3K27me3 and the proliferation marker MIB1 were assessed and correlated with clinical parameters using univariate and multivariate Cox regressions as well as Pearson's chi-squared and log-rank test. Overall, 1268 meningiomas were analyzed with a female to male ratio of 2.6 and a mean age of 58.7 years (range 8.3-91.0). With 163 cases lost to follow up, 1103 cases were available for further analysis with a mean follow-up of 40.3 months (range 1.1-186.3). Male gender, younger age, intracranial tumor localization, progressive tumor, subtotal resection, higher WHO grade, increased MIB1 rate, and loss of H3K27me3 were significant negative prognostic factors in the univariate analysis. H3K27me3 status and all other prognostic factors, except age and tumor location, remained significant in the multivariate model. Furthermore, adjuvant radiotherapy was an independent positive prognostic factor. Loss of H3K27me3 combined with MIB1 labeling index are independent prognostic factors in meningioma. These data from the Tübingen meningioma cohort support the clinical utility of H3K27me3 immunohistochemical staining in meningioma and its integration into the routine histopathological workup.
Sections du résumé
BACKGROUND
A loss of the trimethylation of lysine 27 of histone H3 (H3K27me3) in meningioma has been recently suggested as an adjunct to identify subsets of higher risk of recurrence. The aim of the present study was to assess the prognostic value of H3K27 histone trimethylation and its potential clinical utility in the "Tübingen meningioma cohort."
METHODS
Patients who underwent meningioma resection between October 2003 and December 2015 at the University Hospital Tübingen were included. Immunohistochemical stainings for H3K27me3 and the proliferation marker MIB1 were assessed and correlated with clinical parameters using univariate and multivariate Cox regressions as well as Pearson's chi-squared and log-rank test.
RESULTS
Overall, 1268 meningiomas were analyzed with a female to male ratio of 2.6 and a mean age of 58.7 years (range 8.3-91.0). With 163 cases lost to follow up, 1103 cases were available for further analysis with a mean follow-up of 40.3 months (range 1.1-186.3). Male gender, younger age, intracranial tumor localization, progressive tumor, subtotal resection, higher WHO grade, increased MIB1 rate, and loss of H3K27me3 were significant negative prognostic factors in the univariate analysis. H3K27me3 status and all other prognostic factors, except age and tumor location, remained significant in the multivariate model. Furthermore, adjuvant radiotherapy was an independent positive prognostic factor.
CONCLUSIONS
Loss of H3K27me3 combined with MIB1 labeling index are independent prognostic factors in meningioma. These data from the Tübingen meningioma cohort support the clinical utility of H3K27me3 immunohistochemical staining in meningioma and its integration into the routine histopathological workup.
Identifiants
pubmed: 33367841
pii: 6046432
doi: 10.1093/neuonc/noaa303
pmc: PMC8328015
doi:
Substances chimiques
Histones
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1273-1281Subventions
Organisme : Adolf Leuze Stiftung
Commentaires et corrections
Type : CommentIn
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Neuro-Oncology.
Références
J Neurooncol. 2019 Oct;145(1):125-134
pubmed: 31493161
Acta Neuropathol. 2018 Jun;135(6):955-963
pubmed: 29627952
J Neurosurg. 2018 Jul;129(1):35-47
pubmed: 28984517
J Neurooncol. 2019 Sep;144(3):433-443
pubmed: 31342317
Nat Genet. 2013 Mar;45(3):285-9
pubmed: 23334667
Brain Tumor Pathol. 2015 Jul;32(3):163-8
pubmed: 25930103
Neuro Oncol. 2019 Jul 11;21(7):901-910
pubmed: 31158293
Nat Med. 2011 Mar;17(3):330-9
pubmed: 21386836
Lancet Oncol. 2017 May;18(5):682-694
pubmed: 28314689
Epigenetics. 2017 May 4;12(5):353-369
pubmed: 28059591
Acta Neuropathol. 2020 Sep;140(3):409-413
pubmed: 32642869
Acta Neuropathol. 2016 Jun;131(6):803-20
pubmed: 27157931
Lancet Oncol. 2016 Sep;17(9):e383-91
pubmed: 27599143
J Natl Cancer Inst. 2015 Dec 13;108(5):
pubmed: 26668184
Cell. 2012 Jul 6;150(1):12-27
pubmed: 22770212
Cell. 2020 Jun 11;181(6):1329-1345.e24
pubmed: 32445698
Cell Mol Life Sci. 2018 Jan;75(2):209-223
pubmed: 28717873
Neuro Oncol. 2019 Jan 14;21(Suppl 1):i18-i31
pubmed: 30649489
J Neuropathol Exp Neurol. 2020 Jul 1;79(7):754-762
pubmed: 32447376
Neuro Oncol. 2018 Jan 10;20(1):123-131
pubmed: 29016894
J Hematol Oncol. 2020 Jul 28;13(1):104
pubmed: 32723346
Neuro Oncol. 2019 Nov 1;21(Suppl 5):v1-v100
pubmed: 31675094
Acta Neuropathol. 2017 Nov;134(5):705-714
pubmed: 28733933
Adv Cancer Res. 2016;131:59-95
pubmed: 27451124
J Neurol Neurosurg Psychiatry. 2020 Apr;91(4):378-387
pubmed: 32041819