Evidence map›Paper›PMID 34580720›Full record

ArticleJournal of neuropathology and experimental neurology2021

Molecular Alterations in Meningioangiomatosis Causing Epilepsy.

Antonio Dono, Azim Z Pothiawala, Cole T Lewis, Meenakshi B Bhattacharjee, Leomar Y Ballester, Nitin Tandon

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 31% of its field
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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Antonio DonoVivian L. Smith Department of Neurosurgery, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.ORCID 0000-0002-8041-8399
Azim Z PothiawalaVivian L. Smith Department of Neurosurgery, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.ORCID 0000-0002-4420-6567
Cole T LewisVivian L. Smith Department of Neurosurgery, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.ORCID 0000-0002-2072-4677
Meenakshi B BhattacharjeeDepartment of Pathology and Laboratory Medicine, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.ORCID 0000-0001-7556-9988
Leomar Y BallesterVivian L. Smith Department of Neurosurgery, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.ORCID 0000-0002-6854-6830
Nitin TandonVivian L. Smith Department of Neurosurgery, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.ORCID 0000-0002-2752-2365
Memorial Hermann · USThe University of Texas Health Science Center at Houston · US

Funding

Development and Validation of a CSF Liquid Biopsy for Molecular Characterization and Monitoring of Patients with Central Nervous System TumorsK08CA241651 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BALLESTER, LEOMAR Y · 2020 to 2024
$1.3M
NCI NIH HHS K08 CA241651NIH HHS K08CA241651
6 · The paper itself

Abstract

Meningioangiomatosis (MA) is a rare process at the intersection of cerebral developmental and neoplastic disorders that often results in epilepsy. We evaluated molecular alterations in MA to characterize its biology and pathogenesis. We searched a comprehensive institutional database for patients with MA treated between 2004 and 2019. Demographic, clinical, surgical, and radiographical data were collected. MA and associated meningioma tissues were evaluated using a next-generation sequencing assay interrogating 1425 cancer-related genes. We studied 5 cases: 3 with MA and 2 with MA associated with a meningioma. Of the MAs associated with a meningioma, 1 had deletions in the NF2 gene in both the MA and the meningioma components, whereas the other had an NF2 deletion in only the MA component. Additional mutations were identified in the MA components, suggesting that MA arises from the meningioma rather than the meningioma resulting from a transformation of the MA. The 3 cases of pure MA showed variants of unknown significance with no alterations in known oncogenic drivers. Our findings provide a starting point to a better understanding of the pathogenesis of this rare lesion. Our study indicates that MA-meningiomas have a neoplastic nature that differs from the hamartomatous/developmental nature of pure MA.

Indexed as

AdolescentAdultAge of OnsetBrain NeoplasmsCell Transformation, NeoplasticChild, PreschoolDatabases, FactualEpilepsyFemaleGene DeletionHumansMagnetic Resonance ImagingMaleMeningiomaMutationNeurofibromin 2Neurofibromin 2NF2 protein, humanEpilepsyMeningioangiomatosisMeningiomaMolecular alterationsNF2

Identifiers

PMID34580720
PMCPMC8921655
OpenAlexW3202949354

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.