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. 2020 Jul 9;8(1):104.
doi: 10.1186/s40478-020-00974-x.

The pediatric supratentorial MYCN-amplified high-grade gliomas methylation class presents the same radiological, histopathological and molecular features as their pontine counterparts

A Tauziède-Espariat  1 , M-A Debily  2   3 , D Castel  2   4 , J Grill  2   4 , S Puget  5 , A Roux  6 , R Saffroy  7 , M Pagès  8   9   10   11 , A Gareton  8 , F Chrétien  8 , E Lechapt  8 , V Dangouloff-Ros  12 , N Boddaert  12 , P Varlet  8
Affiliations

The pediatric supratentorial MYCN-amplified high-grade gliomas methylation class presents the same radiological, histopathological and molecular features as their pontine counterparts

A Tauziède-Espariat et al. Acta Neuropathol Commun. .
No abstract available

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Conflict of interest statement

The authors declare that they have no conflict of interest directly related to the topic of this article.

Figures

Fig. 1
Fig. 1
Radiological features of two supratentorial HGG-MYCN. First line: Case 3. (a) T1-weighted images after contrast media injection, (b) T2-weighted images, and (c) diffusion-weighted images: a solid lesion with peri-lesional edema, homogeneous enhancement and hypercellularity (apparent diffusion coefficient (ADC) on diffusion weighted images is restricted in the main part of the tumor). Second line: Case 1. (d) T1-weighted images after contrast media injection, (e) FLAIR-weighted images and (f) cerebral blood flow map using arterial spin labeling: a solid and infiltrative lesion with homogeneous enhancement and high cerebral blood flow
Fig. 2
Fig. 2
Results of the systematic review of supratentorial molecular subgroups of pediatric HGG. a There was no significant difference in terms of progression-free survival (PFS) between HGG-MYCN, HGG-RTKI, supratentorial H3 K27M-mutant HGG and H3 G34-mutant HGG in univariate analysis (p = 0.421). b There was no significant difference in terms of progression-free survival (PFS) between HGG-MYCN, HGG-RTKI, supratentorial H3 K27M-mutant HGG and H3 G34-mutant HGG in univariate analysis (p = 0.109). c There was a significant difference in terms of overall survival (OS) between supratentorial HGG-MYCN and pontine HGG-MYCN in univariate analysis (p < 0.001)
Fig. 3
Fig. 3
Histomolecular features of HGG-MYCN. a Diffuse and solid proliferation with several nodules infiltrating the brain parenchyma (arrowheads) and the leptomeninge with large vessels (asterisk) (Case 2, HPS, × 100 magnification). b Dense proliferation of tumour cells organized in nodules following Virchow-Robin spaces around capillaries (Case 2, HPS, × 250 magnification). c Highly cellular and undifferenciated proliferation composed of alternating fascicles and nodules (Case 2, HPS, × 250 magnification). d Highly malignant tumor with microvascular proliferation (arrowhead) and necrosis (Case 2, HPS, × 400 magnification). e Embryonal proliferation composed of hyperchromatic cells presenting anisocaryotic nuclei with numerous apoptotic bodies (Case 3, HPS, × 400 magnification). f Elevated proliferation index (Case 2, MIB, × 400 magnification). g Diffuse expression of Olig2 (Case 2, × 400 magnification). h Focal expression of GFAP by tumor cells (Case 2, × 400 magnification). i Expression of neurofilament in numerous tumor cells (Case 3, × 400 magnification). j Nuclear accumulation of p53 (Case 2, × 400 magnification). k PTEN loss of expression in tumor cells (endothelial cells as positive internal controls). l High-level of MYCN amplification by FISH analysis with MYCN locus in green signals and control centromeric in red signals (Case 4). Black scale bars represent 1 mm (a), 100 μm (b) and 50 μm (C to K)
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