Evidence map›Paper›PMID 32661686›Full record

ArticleCancer immunology, immunotherapy : CII2021

NF2 mutation status and tumor mutational burden correlate with immune cell infiltration in meningiomas.

John W Rutland, Corey M Gill, Joshua Loewenstern, Hanane Arib, Margaret Pain, Melissa Umphlett, Yayoi Kinoshita, Russell B McBride, Joshua Bederson, Michael Donovan and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  7. The Role of Cytoskeleton Protein 4.1 in Immunotherapy.International journal of molecular sciences · 2023
    Review
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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

13 authors at 3 institutions in 1 country.

John W Rutland *Department of Neurosurgery, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue; Floor 8, New York, NY, 10129, USA. jack.rutland@icahn.mssm.edu.ORCID http://orcid.org/0000-0002-6412-6708
Corey M Gill *Department of Neurosurgery, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue; Floor 8, New York, NY, 10129, USA.
Joshua LoewensternDepartment of Neurosurgery, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue; Floor 8, New York, NY, 10129, USA.
Hanane AribDepartment of Genetics and Genomic Sciences, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Margaret PainDepartment of Neurosurgery, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue; Floor 8, New York, NY, 10129, USA.
Melissa UmphlettDepartment of Pathology, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Yayoi KinoshitaDepartment of Pathology, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Russell B McBrideDepartment of Pathology, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Joshua BedersonDepartment of Neurosurgery, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue; Floor 8, New York, NY, 10129, USA.
Michael DonovanDepartment of Pathology, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Robert SebraDepartment of Genetics and Genomic Sciences, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Raj K ShrivastavaDepartment of Neurosurgery, Icahn School of Medicine At Mount Sinai, 1468 Madison Avenue; Floor 8, New York, NY, 10129, USA.
Mary FowkesDepartment of Pathology, Icahn School of Medicine At Mount Sinai, New York, NY, USA.
Faculty of 1000 (United States) · USIcahn School of Medicine at Mount Sinai · USSema4 (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe tumor microenvironment is an emerging biomarker of underlying genomic heterogeneity and response to immunotherapy-based treatment regimens in solid malignancies. How tumor mutational burden influences the density, distribution, and presence of a localized immune response in meningiomas is unknown.

methodsRepresentative hematoxylin and eosin slides were reviewed at 40X to assess for the density of inflammatory cells. Lymphocytes and macrophages were quantified in the following ordinal manner: 0 = not present, 1 = 1-25 cells present, and 2 = greater than 26 cells present. Immune cell infiltrate grade was scored for both scattered and aggregated distributions. Next generation targeted sequencing was performed on all meningiomas included in this study.

resultsOne hundred and forty-five meningiomas were evaluated in this study. Lymphocytes were observed in both scattered (95.9%) and aggregated (21.4%) distributions. A total of 115 (79.3%) meningiomas had 1-25 scattered lymphocytes, and 24 (16.6%) had > 25 scattered lymphocytes, and 6 (4.1%) had no scattered lymphocytes. Twenty (13.8%) meningiomas had 1-25 aggregated lymphocytes. Eleven (7.6%) had > 25 aggregated lymphocytes and 114 (78.6%) had no aggregated lymphocytes. Six (4.1%) meningiomas had 1-25 aggregated macrophages, 5 (3.4%) had > 25 aggregated macrophages, and 134 (92.4%) had no aggregated macrophages. Density of aggregated lymphocytes and aggregated macrophages were associated with higher tumor grade, P = 0.0071 and P = 0.0068, respectively. Scattered lymphocyte density was not associated with meningioma grade. The presence of scattered lymphocytes was associated with increased tumor mutational burden. Meningiomas that did not have scattered lymphocytes had a mean number of single mutations of 2.3 ± 2.9, compared with meningiomas that had scattered lymphocytes, 6.9 ± 20.3, P = 0.03. NF2 mutations were identified in 59 (40.7%) meningiomas and were associated with increased density of scattered lymphocytes. NF2 mutations were seen in 0 (0%) meningiomas that did not have scattered lymphocytes, 46 (40.0%) meningiomas that had 1-25 scattered lymphocytes, and 13 (54.2%) meningiomas that had > 25 scattered lymphocytes, P = 0.046.

conclusionsOur findings suggest that distribution of immune cell infiltration in meningiomas is associated with tumor mutational burden. NF2 mutational status was associated with an increasing density of scattered lymphocytes. As the role of immunotherapy in meningiomas continues to be elucidated with clinical trials that are currently underway, these results may serve as a novel biomarker of tumor mutational burden in meningiomas.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorFemaleGenomicsHumansLymphocytesMacrophagesMaleMeningeal NeoplasmsMeningiomaMiddle AgedMutationNeurofibromin 2Tumor MicroenvironmentBiomarkers, TumorNeurofibromin 2NF2 protein, humanBiomarkerImmunotherapyInflammationMeningiomaSequencing

Identifiers

PMID32661686
PMCPMC10991085
OpenAlexW3043333669

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.