Concordant with latest books, the median age of our patients was 3.7 (1 to 7?years old) and concerned 4 ladies (Cases 2, 3, 4 and 6) and 2 males Baicalein (Cases 1 and 5) [1]. Clinically, all our patients presented similarly to midline diffuse gliomas, H3K27?M-mutant, with a short clinical history ( ?6?months of symptom period) and the presence of a pontine tumour infiltrating at least 50% of the pons. Radiologically, all tumors were centered in the pons, with variable involvement of the mesencephalon and the middle cerebellar peduncle. None was calcified nor hemorrhagic. HGG-MYCN displayed necrosis at first presentation, with annular enhancement, larger than in H3K27?M gliomas. Furthermore, diffusion was more restricted than classically reported in diffuse intrinsic pontine gliomas (mutations found by WES. EGFR overexpression (Cases 3 and 6) and loss of PTEN (Cases 2 and 5) were mutually unique. No mutations of the promoter, and were observed. The amplification of the gene was confirmed by FISH analysis Zytoamplification is not a specific alteration of the HGG-MYCN entity. Indeed, it may be encountered in a small portion of pediatric glioblastoma-RTKI (Receptor of Tyrosine Kinase I) and CRTKII (Receptor of Tyrosine Kinase II) [6]. However, WES analysis revealed a co-amplification of the gene in all our cases which is not described in other types of glioblastomas. This co-amplification was explained in the supra-tentorial and the pontine location of HGG-MYCN [1, 9]. encodes the protein ID2 (Inhibitor of DNA-binding 2) which is usually portrayed by oligodendroglial precursor cells, a progenitor cell type implicated in the oncogenesis of gliomas [4, 7, 11]. Furthermore, a subset of diffuse midline gliomas with H3.3-K27?M mutations overexpress without amplification of the gene [1]. These data recommend a potential common Seafood evaluation in the diagnostic immunohistochemical/molecular -panel of pediatric brainstem tumours, to H3K27M similarly, Lin28A and INI1/BRG1 antibodies for the differential diagnoses of DIPG, ETMR and AT/RT, respectively. Funding The authors declare they have received funding to finance the sequencing analyses from Etoile de Martin et Les Boucles du C?ur de la Fondation Carrefour for the project Imagine and RARE for Margo for BIOMEDE. Authors contributions ATE, MAD, DC, JG, SP, MS, KB, AG, VDR, Un, PV and NB participated in conception, style, set up and assortment of data, data interpretation and analysis, manuscript approval and writing. DC and MAD performed WES analyses. NB and VDR compiled radiological data. JG participated by giving study components or patient details. All authors accepted and browse the last manuscript. Competing interests The authors declare they have no competing interests. Publishers Note Springer Nature continues to be neutral in regards to to jurisdictional promises in published maps and institutional affiliations.. of and (2 situations from BIOMEDE cohort) [3]. Herein, our purpose is to describe the medical, imaging, histopathological, immunohistochemical and molecular features of Baicalein these instances to better characterize them. Concordant with recent literature, the Baicalein median age of our individuals was 3.7 (1 to 7?years old) and concerned 4 ladies (Instances 2, 3, 4 and 6) and 2 Baicalein kids (Instances 1 and 5) [1]. Clinically, all our individuals presented similarly to midline diffuse gliomas, H3K27?M-mutant, with a short clinical history ( ?6?weeks of symptom period) and the presence of a pontine tumour infiltrating at least 50% of the pons. Radiologically, all tumors were centered in the pons, with variable involvement of the mesencephalon and the middle cerebellar peduncle. None was calcified nor hemorrhagic. HGG-MYCN displayed necrosis at first demonstration, with annular enhancement, larger than in H3K27?M gliomas. Furthermore, diffusion was more restricted than classically reported in diffuse intrinsic pontine gliomas (mutations found by WES. EGFR overexpression (Instances 3 and 6) and loss of PTEN (Instances 2 and 5) were mutually unique. No mutations of the promoter, and were observed. The amplification of the gene was confirmed by FISH Baicalein analysis Zytoamplification is not a specific alteration of the HGG-MYCN entity. Indeed, it may be experienced in a small portion of pediatric glioblastoma-RTKI (Receptor of Tyrosine Kinase I) and CRTKII (Receptor of Tyrosine Kinase II) [6]. However, WES CANPml analysis exposed a co-amplification of the gene in all our instances which is not described in other types of glioblastomas. This co-amplification was explained in the supra-tentorial and the pontine location of HGG-MYCN [1, 9]. encodes the protein ID2 (Inhibitor of DNA-binding 2) which is definitely indicated by oligodendroglial precursor cells, a progenitor cell type implicated in the oncogenesis of gliomas [4, 7, 11]. Furthermore, a subset of diffuse midline gliomas with H3.3-K27?M mutations overexpress without amplification of this gene [1]. These data suggest a potential common FISH analysis in the diagnostic immunohistochemical/molecular panel of pediatric brainstem tumours, similarly to H3K27M, INI1/BRG1 and Lin28A antibodies for the differential diagnoses of DIPG, AT/RT and ETMR, respectively. Funding The authors declare that they have received funding to financing the sequencing analyses from Etoile de Martin et Les Boucles du C?ur de la Fondation Carrefour for the project RARE and Imagine for Margo for BIOMEDE. Authors contributions ATE, MAD, DC, JG, SP, MS, KB, AG, VDR, EL, NB and PV participated in conception, design, collection and assembly of data, data analysis and interpretation, manuscript writing and authorization. MAD and DC performed WES analyses. VDR and NB compiled radiological data. JG participated by providing study materials or patient info. All authors read and accepted the ultimate manuscript. Competing passions The writers declare they have no contending interests. Publishers Be aware Springer Nature continues to be neutral in regards to to jurisdictional promises in released maps and institutional affiliations..