Evidence map›Paper›PMID 28552950›Full record

ArticlePloS one2017

Genomic profile of human meningioma cell lines.

Yu Mei, Wenya Linda Bi, Noah F Greenwald, Nathalie Y Agar, Rameen Beroukhim, Gavin P Dunn, Ian F Dunn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 3 pooled it
3.5field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 3 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Review
  5. 'AnbioRxiv : the preprint server for biology · 2026
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  18. Preclinical Models of Meningioma.Advances in experimental medicine and biology · 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

7 authors at 3 institutions in 1 country.

Yu MeiCenter for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.ORCID http://orcid.org/0000-0001-9865-1765
Wenya Linda BiCenter for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Noah F GreenwaldCenter for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Nathalie Y AgarCenter for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Rameen BeroukhimDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
Gavin P DunnDepartment of Neurosurgery, Pathology, and Immunology, Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Ian F DunnCenter for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Brigham and Women's Hospital · USBroad Institute · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Meningiomas, derived from arachnoid cap cells, are the most common intracranial tumor. High-grade meningiomas, as well as those located at the skull base or near venous sinuses, frequently recur and are challenging to manage. Next-generation sequencing is identifying novel pharmacologic targets in meningiomas to complement surgery and radiation. However, due to the lack of in vitro models, the importance and implications of these genetic variants in meningioma pathogenesis and therapy remain unclear. We performed whole exome sequencing to assess single nucleotide variants and somatic copy number variants in four human meningioma cell lines, including two benign lines (HBL-52 and Ben-Men-1) and two malignant lines (IOMM-Lee and CH157-MN). The two malignant cell lines harbored an elevated rate of mutations and copy number alterations compared to the benign lines, consistent with the genetic profiles of high-grade meningiomas. In addition, these cell lines also harbored known meningioma driver mutations in neurofibromin 2 (NF2) and TNF receptor-associated factor 7 (TRAF7). These findings demonstrate the relevance of meningioma cell lines as a model system, especially as tools to investigate the signaling pathways of, and subsequent resistance to, therapeutics currently in clinical trials.

Indexed as

GenomicsCell Line, TumorDNA Copy Number VariationsHumansMeningeal NeoplasmsMeningiomaMutation

Identifiers

PMID28552950
PMCPMC5446134
OpenAlexW2618061473

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.