Evidence map›Paper›PMID 39228008›Full record

ArticleActa neuropathologica communications2024

Concurrent ependymal and ganglionic differentiation in a subset of supratentorial neuroepithelial tumors with EWSR1-PLAGL1 rearrangement.

Julieann C Lee, Selene C Koo, Larissa V Furtado, Alex Breuer, Mohammad K Eldomery, Asim K Bag, Pat Stow, Gary Rose, Trisha Larkin, Rick Sances and 12 more

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

22 authors.

Julieann C LeeDepartment of Pathology, Neuropathology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA. Julieann.lee@stjude.org.
Selene C KooDepartment of Pathology, Molecular Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Larissa V FurtadoDepartment of Pathology, Molecular Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Alex BreuerDepartment of Pathology, Molecular Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Mohammad K EldomeryDepartment of Pathology, Molecular Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Asim K BagDepartment of Diagnostic Imaging, St. Jude Children's Research Hospital, Memphis, TN, USA.
Pat StowDepartment of Pathology, Molecular Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Gary RoseDepartment of Pathology, Nemours Children's Hospital, Wilmington, DE, USA.
Trisha LarkinDepartment of Pediatrics, St. Joseph's Hospital, Tampa, FL, USA.
Rick SancesDepartment of Pathology, East TN Children's Hospital, Knoxville, TN, USA.
Bette K Kleinschmidt-DeMastersDepartment of Pathology, University of Colorado, Denver, CO, USA.
Jenna L BodmerDepartment of Pathology, University of Colorado, Denver, CO, USA.
Nicholas WillardDepartment of Pathology, University of Colorado, Denver, CO, USA.
Murat GokdenDepartment of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Sonika DahiyaDivision of Neuropathology, Department of Pathology and Immunology, Washington University, St. Louis, MO, USA.
Kaleigh RobertsDivision of Neuropathology, Department of Pathology and Immunology, Washington University, St. Louis, MO, USA.
Kelsey C BertrandDepartment of Oncology, Division of Neuro-Oncology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Daniel C MoreiraDepartment of Oncology, Division of Neuro-Oncology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Giles W RobinsonDepartment of Oncology, Division of Neuro-Oncology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Jun Qin MoDepartment of Pathology, Rady Children's Hospital, University of California School of Medicine, San Diego, CA, USA.
David W EllisonDepartment of Pathology, Neuropathology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.
Brent A OrrDepartment of Pathology, Neuropathology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroepithelial tumors with fusion of PLAGL1 or amplification of PLAGL1/PLAGL2 have recently been described often with ependymoma-like or embryonal histology respectively. To further evaluate emerging entities with PLAG-family genetic alterations, the histologic, molecular, clinical, and imaging features are described for 8 clinical cases encountered at St. Jude (EWSR1-PLAGL1 fusion n = 6; PLAGL1 amplification n = 1; PLAGL2 amplification n = 1). A histologic feature observed on initial resection in a subset (4/6) of supratentorial neuroepithelial tumors with EWSR1-PLAGL1 rearrangement was the presence of concurrent ependymal and ganglionic differentiation. This ranged from prominent clusters of ganglion cells within ependymoma/subependymoma-like areas, to interspersed ganglion cells of low to moderate frequency among otherwise ependymal-like histology, or focal areas with a ganglion cell component. When present, the combination of ependymal-like and ganglionic features within a supratentorial neuroepithelial tumor may raise consideration for an EWSR1-PLAGL1 fusion, and prompt initiation of appropriate molecular testing such as RNA sequencing and methylation profiling. One of the EWSR1-PLAGL1 fusion cases showed subclonal INI1 loss in a region containing small clusters of rhabdoid/embryonal cells, and developed a prominent ganglion cell component on recurrence. As such, EWSR1-PLAGL1 neuroepithelial tumors are a tumor type in which acquired inactivation of SMARCB1 and development of AT/RT features may occur and lead to clinical progression. In contrast, the PLAGL2 and PLAGL1 amplified cases showed either embryonal histology or contained an embryonal component with a significant degree of desmin staining, which could also serve to raise consideration for a PLAG entity when present. Continued compilation of associated clinical data and histopathologic findings will be critical for understanding emerging entities with PLAG-family genetic alterations.

Indexed as

RNA-Binding Protein EWSSupratentorial NeoplasmsTranscription FactorsAdolescentAdultCell Cycle ProteinsCell DifferentiationChildChild, PreschoolChromosomal Proteins, Non-HistoneDNA-Binding ProteinsEpendymaFemaleGene RearrangementHumansMaleCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsEWSR1 protein, humanOncogene Proteins, FusionPLAGL1 protein, humanRNA-Binding Protein EWSTranscription FactorsTumor Suppressor ProteinsEpendymal-likeEWSR1-PLAGL1Ganglionic differentiationNeuroepithelial tumorPLAGL1PLAGL2

Identifiers

PMID39228008
PMCPMC11370057

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