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. 2020 Mar 9;8:27. doi: 10.1186/s40478-020-00904-x

Fig. 1.

Fig. 1

Histopathologically and genetically defined LEAT. Legend to Figure: Selected LEAT entities in which a common gene driving mutation has been discovered. a-d: a papillary glio-neuronal tumor (PGNT) with the characteristic presentation of papillary growth pattern (A – HE), glial (B – GFAP) and neuronal components (C – MAP2 and D – Synaptophysin). This tumor was included in the study by Hou et al. describing its distinct DNA methylation profile and SLC44A1-PRKCA fusion [31]. e-h: a dysembryoplastic neuroepithelial tumor (DNT) with the characteristic histological presentation of a specific glio-neuronal element (E – HE), lack of GFAP immunoreactivity in the clear-cell component (F - GFAP), floating neurons (G – MAP2) and a newly discovered p16 immunoreactivity shown in H, helpful to distinguish the DNT from other LEAT entities (unpublished observation, courtesy of Dr. Roland Coras, Erlangen, Germany). This tumor would typically present as FGFR1 altered CD34 negative DNT (not yet genetically confirmed in this tumor sample). j-m: a ganglioglioma (GG) with a characteristic glial-neuronal phenotype and small calcifications (J – HE), a predominant astroglial component (K-GFAP), dysplastic neurons (L-MAP2) and CD34 immunoreactivity in the tumor mass lesion shown in lower right corner as well as in diffusely infiltrated peritumoral grey and white matter (M-CD34). This tumor was included in the study of Blumcke et al. describing the distinct DNA methylation patterns of BRAF V600E mutated CD34 positive GG vs. CD34 negative DNT [3]. n-r: an angiocentric glioma (AG) with characteristic growth pattern around blood vessels (N-HE), a predominant astroglial phenotype (O-GFAP), enriched neuronal matrix (P-MAP2) and EMA-dots similar to ependymoma (R-EMA). This tumor showed a MYB fusion as previously described by Qaddomi et al. [58]. s-w: an isomorphic and diffusely infiltrating glioma (IDG) of low cellularity (S-HE), a predominant astroglial phenotype (T-GFAP), only few contained and pre-existing neurons (U-MAP2) and lack of IDH1R132H mutations (W-IDH mutation specific antibody). This tumor showed a MYBL1 fusion and was previously described by Wefers et al. [75]