about
The role of histone modifications and telomere alterations in the pathogenesis of diffuse gliomas in adults and children.Imaging Characteristics of Pediatric Diffuse Midline Gliomas with Histone H3 K27M Mutation.Multimodal molecular analysis of astroblastoma enables reclassification of most cases into more specific molecular entities.Adenomatoid tumors of the male and female genital tract are defined by TRAF7 mutations that drive aberrant NF-kB pathway activation.Diffuse midline gliomas with subclonal H3F3A K27M mutation and mosaic H3.3 K27M mutant protein expression.Genetic confirmation that ependymoma can arise as part of multiple endocrine neoplasia type 1 (MEN1) syndrome.Deep sequencing of WNT-activated medulloblastomas reveals secondary SHH pathway activation.Multinodular and vacuolating neuronal tumor of the cerebrum is a clonal neoplasm defined by genetic alterations that activate the MAP kinase signaling pathway.STAG2 deficiency induces interferon responses via cGAS-STING pathway and restricts virus infection.A recurrent kinase domain mutation in PRKCA defines chordoid glioma of the third ventricle.The genetic landscape of ganglioglioma.Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma.Oligodendrogliomas, IDH-mutant and 1p/19q-codeleted, arising during teenage years often lack TERT promoter mutation that is typical of their adult counterpartsA requirement for STAG2 in replication fork progression creates a targetable synthetic lethality in cohesin-mutant cancersThe genetic landscape of gliomas arising after therapeutic radiationWell-differentiated papillary mesothelioma of the peritoneum is genetically defined by mutually exclusive mutations in TRAF7 and CDC42.An update on the central nervous system manifestations of familial tumor predisposition syndromesRecurrent non-canonical histone H3 mutations in spinal cord diffuse gliomasMyxoid glioneuronal tumor of the septum pellucidum and lateral ventricle is defined by a recurrent PDGFRA p.K385 mutation and DNT-like methylation profileGliomas arising in the setting of Li-Fraumeni syndrome stratify into two molecular subgroups with divergent clinicopathologic featuresMyxoid glioneuronal tumor, PDGFRA p.K385-mutant: clinical, radiologic, and histopathologic featuresInfant high grade gliomas comprise multiple subgroups characterized by novel targetable gene fusions and favorable outcomesPrimary intracranial sarcomas with DICER1 mutation often contain prominent eosinophilic cytoplasmic globules and can occur in the setting of neurofibromatosis type 1Diffusion Characteristics of Pediatric Diffuse Midline Gliomas with Histone H3-K27M Mutation Using Apparent Diffusion Coefficient Histogram AnalysisClinicopathologic and molecular features of intracranial desmoplastic small round cell tumorsPreoperative MR Imaging to Differentiate Chordoid Meningiomas from Other Meningioma Histologic SubtypesPediatric bithalamic gliomas have a distinct epigenetic signature and frequent EGFR exon 20 insertions resulting in potential sensitivity to targeted kinase inhibitioncIMPACT-NOW update 6: new entity and diagnostic principle recommendations of the cIMPACT-Utrecht meeting on future CNS tumor classification and gradingHigh-grade neuroepithelial tumor with BCOR exon 15 internal tandem duplication-a comprehensive clinical, radiographic, pathologic, and genomic analysisRecurrent KBTBD4 small in-frame insertions and absence of DROSHA deletion or DICER1 mutation differentiate pineal parenchymal tumor of intermediate differentiation (PPTID) from pineoblastomaMultiregion exome sequencing of ovarian immature teratomas reveals 2N near-diploid genomes, paucity of somatic mutations, and extensive allelic imbalances shared across mature, immature, and disseminated componentsClinicopathologic features of anaplastic myxopapillary ependymomas
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P50
description
researcher
@en
wetenschapper
@nl
name
David A Solomon
@en
David A Solomon
@nl
type
label
David A Solomon
@en
David A Solomon
@nl
prefLabel
David A Solomon
@en
David A Solomon
@nl
P31
P496
0000-0003-4571-7999