Evidence map›Paper›PMID 38699943›Full record

ArticleJournal of neuropathology and experimental neurology2024

Ganglioglioma with anaplastic/high-grade transformation: Histopathologic, molecular, and epigenetic characterization of 3 cases.

M Adelita Vizcaino, Caterina Giannini, Daniel Lalich, Ali Nael, Robert B Jenkins, Quynh Tran, Brent A Orr, Zied Abdullaev, Kenneth Aldape, Rachael A Vaubel

Abstract readCase Reports
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

M Adelita VizcainoDepartment of Laboratory Medicine and Pathology, Mayo Clinic Rochester, Minnesota, USA.ORCID 0000-0003-4636-8743
Caterina GianniniDepartment of Laboratory Medicine and Pathology, Mayo Clinic Rochester, Minnesota, USA.ORCID 0000-0003-2757-6782
Daniel LalichDepartment of Pathology, Robert J. Dole VA Medical Center and Wesley Healthcare Center, Wichita, Kansas, USA.
Ali NaelDepartment of Pathology, Children's Hospital of Orange County and University of California Irvine, Orange County, California, USA.
Robert B JenkinsDepartment of Laboratory Medicine and Pathology, Mayo Clinic Rochester, Minnesota, USA.
Quynh TranDepartment of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
Brent A OrrDepartment of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
Zied AbdullaevLaboratory of Pathology, National Cancer Institute/Center for Cancer Research, Bethesda, Maryland, USA.
Kenneth AldapeLaboratory of Pathology, National Cancer Institute/Center for Cancer Research, Bethesda, Maryland, USA.ORCID 0000-0001-5119-7550
Rachael A VaubelDepartment of Laboratory Medicine and Pathology, Mayo Clinic Rochester, Minnesota, USA.ORCID 0000-0001-8842-5975

Funding

Mayo Clinic Department of Laboratory Medicine and Pathology
6 · The paper itself

Abstract

Ganglioglioma (GG) with anaplasia (anaplastic ganglioglioma) is a rare and controversial diagnosis. When present, anaplasia involves the glial component of the tumor, either at presentation or at recurrence. To date, most published cases lack molecular characterization. We describe the histologic and molecular features of 3 patients presenting with BRAF p. V600E-mutant GG (CNS WHO grade 1) with high-grade glial transformation at recurrence. The tumors occurred in pediatric patients (age 9-16 years) with time to recurrence from 20 months to 7 years. At presentation, each tumor was low-grade, with a BRAFV600E-positive ganglion cell component and a glial component resembling pleomorphic xanthoastrocytoma (PXA) or fibrillary astrocytoma. At recurrence, tumors resembled anaplastic PXA or high-grade astrocytomas without neuronal differentiation. CDKN2A homozygous deletion (HD) was absent in all primary tumors. At recurrence, 2 cases acquired CDKN2A HD; the third case showed loss of p16 and MTAP immunoexpression, but no CDKN2A/B HD or mutation was identified. By DNA methylation profiling, all primary and recurrent tumors either grouped or definitely matched to different methylation classes. Our findings indicate that malignant progression of the glial component can occur in GG and suggest that CDKN2A/B inactivation plays a significant role in this process.

Indexed as

Brain NeoplasmsGangliogliomaAdolescentCell Transformation, NeoplasticChildEpigenesis, GeneticFemaleHumansMaleNeoplasm Recurrence, LocalProto-Oncogene Proteins B-rafBRAF protein, humanProto-Oncogene Proteins B-rafAnaplasiaBRAF p. V600E-mutantCDKN2A/B inactivationGangliogliomaMethylation class PXAWhole-genome DNA methylation profiling

Identifiers

PMID38699943
PMCPMC12104497

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.