The molecular pattern of histopathological progression to anaplastic meningioma - A case report

被引:2
|
作者
Och, Waldemar [1 ]
Kulbacki, Kamil [1 ]
Szostak, Blazej [2 ]
Sikorska, Beata [3 ]
Zakrzewska, Magdalena [3 ]
Szmuda, Tomasz [4 ]
Liberski, Pawel P. [3 ]
Budzisz, Tomasz [1 ]
机构
[1] Reg Specialist Hosp, Dept Neurosurg, Olsztyn, Poland
[2] Reg Specialist Hosp, Dept Pathol, Olsztyn, Poland
[3] Med Univ Lodz, Dept Mol Pathol & Neuropathol, Lodz, Poland
[4] Med Univ Gdansk, Dept Neurosurg, Debinki 7, PL-81952 Gdansk, Poland
关键词
Meningioma; Anaplastic meningioma; Molecular biology; Loss of heterozygosity; Tumour progression; MALIGNANT PROGRESSION; TUMOR-SUPPRESSOR; CLASSIFICATION; RECURRENCE; HETEROZYGOSITY; EXPRESSION; PATHWAYS; DELETION; GENETICS;
D O I
10.1016/j.pjnns.2016.03.008
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Meningiomas (MGs) are the most frequent primary tumours of the central nervous system (CNS) and exhibit a large spectrum of histological types and clinical phenotypes. The WHO classification of CNS tumours established strict diagnostic criteria of the benign (Grade 1), atypical (Grade 2) and anaplastic (Grade 3) subtypes. Combined with the resection rate, WHO grading has the most crucial role as the prognostic factor. Additionally, such biomarkers as Ki-67/MIB-1, progesterone receptors and phosphor-histone H3 were correlated with MG progression. Recently, it was suggested that the aggressive behaviour of some MGs is attributed to molecular alterations, regardless of their histopathology. The analysis of loss of heterozygosity (LOH) at chromosomes 1, 9, 10, 14 and 22 was performed. The presented case of WHO Grade 2 MG initially exhibited LOH at chromosomes 10, 14 and 22. In the first recurrence, the tumour genetic profiling revealed additional LOH at chromosome 1p and atypical histopathology. During the second recurrence, an aggressive phenotype was observed and tumour progressed to an anaplastic form. Considering the appearance of the tumour relapses, the set of molecular changes overtook the histopathological progression. The genetic and histopathological imbalance in the tumour progression in secondary anaplastic MGs has not been previously described. The evolution of genetic and histopathological changes was presented in the same patient. In the future, the individualised therapy of potentially more aggressive forms of MGs could be based on certain chromosome aberrations. (C) 2016 Polish Neurological Society. Published by Elsevier Sp. z o.o. All rights reserved.
引用
收藏
页码:288 / 293
页数:6
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