Data on unveiling the occurrence of transient, multi-contaminated mafic magmas inside a rhyolitic reservoir feeding an explosive eruption (Nisyros, Greece).

This data article includes the description and the geochemical and mineralogical dataset of 67 pyroclastic rock samples from the Upper Pumice (UP) explosive activity of Nisyros volcano (eastern South Aegean Active Volcanic Arc). A detailed field and petrographic description of the studied outcrops and samples are reported, including representative photomicrographs and SEM images, whole-rock major and trace elements compositions of 31 representative samples and Sr-Nd isotope ratios on 22 selected samples. Analytical methods and conditions used for data acquisition are also reported. The UP eruption produced a stratigraphic sequence constituted by a basal fallout deposit, gradually substituted by pyroclastic density current (PDC) deposits; these are overlaid by a lag-breccia unit, and the sequence is closed by a grey ash flow level. The juvenile is mainly constituted by white-yellow, moderately crystalline pumice with rhyolitic composition and homogenous Sr-Nd isotope values. Variable amounts of dense, grey, crystalline juvenile lapilli clasts (CRC, Crystal-Rich Clast), with rounded shape and less evolved composition (andesite to dacite) are also present in the deposit. These mafic CRCs are peculiar due to their large variability in textures (from distinctive diktytaxitic to strongly fragmented structure without a defined fabric) and in the geochemical and isotopic composition. The data acquired were fundamental to reconstruct the complex and peculiar history of ascent, storage and differentiation/assimilation processes of these mafic melts before their intrusion into the shallow, rhyolitic magma chamber, with important implication on the possible eruption trigger during the more recent explosive phase of activity at Nisyros volcano. Moreover, the geochemical and isotopic analyses provide new original data to the general knowledge of the Aegean volcanics. All the data reported in this paper are related to the research article Braschi et al. (2022).

Isomorphic diffuse glioma is a morphologically and molecularly distinct tumour entity with recurrent gene fusions of MYBL1 or MYB and a benign disease course.

The "isomorphic subtype of diffuse astrocytoma" was identified histologically in 2004 as a supratentorial, highly differentiated glioma with low cellularity, low proliferation and focal diffuse brain infiltration. Patients typically had seizures since childhood and all were operated on as adults. To define the position of these lesions among brain tumours, we histologically, molecularly and clinically analysed 26 histologically prototypical isomorphic diffuse gliomas. Immunohistochemically, they were GFAP-positive, MAP2-, OLIG2- and CD34-negative, nuclear ATRX-expression was retained and proliferation was low. All 24 cases sequenced were IDH-wildtype. In cluster analyses of DNA methylation data, isomorphic diffuse gliomas formed a group clearly distinct from other glial/glio-neuronal brain tumours and normal hemispheric tissue, most closely related to paediatric MYB/MYBL1-altered diffuse astrocytomas and angiocentric gliomas. Half of the isomorphic diffuse gliomas had copy number alterations of MYBL1 or MYB (13/25, 52%). Gene fusions of MYBL1 or MYB with various gene partners were identified in 11/22 (50%) and were associated with an increased RNA-expression of the respective MYB-family gene. Integrating copy number alterations and available RNA sequencing data, 20/26 (77%) of isomorphic diffuse gliomas demonstrated MYBL1 (54%) or MYB (23%) alterations. Clinically, 89% of patients were seizure-free after surgery and all had a good outcome. In summary, we here define a distinct benign tumour class belonging to the family of MYB/MYBL1-altered gliomas. Isomorphic diffuse glioma occurs both in children and adults, has a concise morphology, frequent MYBL1 and MYB alterations and a specific DNA methylation profile. As an exclusively histological diagnosis may be very challenging and as paediatric MYB/MYBL1-altered diffuse astrocytomas may have the same gene fusions, we consider DNA methylation profiling very helpful for their identification.

Tumors diagnosed as cerebellar glioblastoma comprise distinct molecular entities.

In this multi-institutional study we compiled a retrospective cohort of 86 posterior fossa tumors having received the diagnosis of cerebellar glioblastoma (cGBM). All tumors were reviewed histologically and subjected to array-based methylation analysis followed by algorithm-based classification into distinct methylation classes (MCs). The single MC containing the largest proportion of 25 tumors diagnosed as cGBM was MC anaplastic astrocytoma with piloid features representing a recently-described molecular tumor entity not yet included in the WHO Classification of Tumours of the Central Nervous System (WHO classification). Twenty-nine tumors molecularly corresponded to either of 6 methylation subclasses subsumed in the MC family GBM IDH wildtype. Further we identified 6 tumors belonging to the MC diffuse midline glioma H3 K27 M mutant and 6 tumors allotted to the MC IDH mutant glioma subclass astrocytoma. Two tumors were classified as MC pilocytic astrocytoma of the posterior fossa, one as MC CNS high grade neuroepithelial tumor with BCOR alteration and one as MC control tissue, inflammatory tumor microenvironment. The methylation profiles of 16 tumors could not clearly be assigned to one distinct MC. In comparison to supratentorial localization, the MC GBM IDH wildtype subclass midline was overrepresented, whereas the MCs GBM IDH wildtype subclass mesenchymal and subclass RTK II were underrepresented in the cerebellum. Based on the integration of molecular and histological findings all tumors received an integrated diagnosis in line with the WHO classification 2016. In conclusion, cGBM does not represent a molecularly uniform tumor entity, but rather comprises different brain tumor entities with diverse prognosis and therapeutic options. Distinction of these molecular tumor classes requires molecular analysis. More than 30% of tumors diagnosed as cGBM belong to the recently described molecular entity of anaplastic astrocytoma with piloid features.