Evidence map›Paper›PMID 17962031›Full record

ArticleNeurobiology of disease2008

Modeling NF2 with human arachnoidal and meningioma cell culture systems: NF2 silencing reflects the benign character of tumor growth.

Marianne F James, Johanna M Lelke, Mia Maccollin, Scott R Plotkin, Anat O Stemmer-Rachamimov, Vijaya Ramesh, James F Gusella

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Preclinical Models of Meningioma.Advances in experimental medicine and biology · 2023
    Review
  5. Tumor-Derived Cell Culture Model for the Investigation of Meningioma Biology.Journal of neuropathology and experimental neurology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Cerebrospinal Fluid Hyaluronan and Neurofibromatosis Type 2.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Marianne F JamesMolecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Richard B. Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA.
Johanna M Lelke
Mia Maccollin
Scott R Plotkin
Anat O Stemmer-Rachamimov
Vijaya Ramesh
James F Gusella
Massachusetts General Hospital · US

Funding

Vector Query and Therapy For TSC and NF2 LesionsP01NS024279 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI KWIATKOWSKI, DAVID J. · 1987 to 2012
$14.7M
Interdepartmental Neuroscience CenterP30NS045776 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BREAKEFIELD, XANDRA OWENS, TANNOUS, BAKHOS A · 2003 to 2018
$11.1M
CHARACTERIZATION OF TSC PROTEIN HAMARTIN AND TUBERINR01NS041917 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI RAMESH, VIJAYA · 2001 to 2005
$865k
NINDS NIH HHS NS024279NINDS NIH HHS NS041917NINDS NIH HHS NS045776NINDS NIH HHS P01 NS024279NINDS NIH HHS P30 NS045776NINDS NIH HHS R01 NS041917
6 · The paper itself

Abstract

Meningiomas, common tumors arising from arachnoidal cells of the meninges, may occur sporadically, or in association with the inherited disorder, neurofibromatosis 2 (NF2). Most sporadic meningiomas result from NF2 inactivation, resulting in loss of tumor suppressor merlin, implicated in regulating membrane-cytoskeletal organization. To investigate merlin function in an authentic target cell type for NF2 tumor formation, we established primary cultures from genetically-matched meningioma and normal arachnoidal tissues. Our studies revealed novel and distinct cell biological and biochemical properties unique to merlin-deficient meningioma cells compared to merlin-expressing arachnoidal and meningioma cells, and other NF2-deficient cell types. Merlin-deficient meningioma cells displayed cytoskeletal and cell contact defects, altered cell morphology and growth properties, most notably cell senescence, implicating the activation of senescence pathways in limiting benign meningioma growth. Merlin suppression by RNAi in arachnoidal cells replicated merlin-deficient meningioma features, thus establishing these cell systems as disease-relevant models for studying NF2 tumorigenesis.

Indexed as

ActinsArachnoidBromodeoxyuridineCateninsCell ProliferationCells, CulturedCytoskeletonGene Expression Regulation, NeoplasticGenes, Neurofibromatosis 2HumansMembrane ProteinsMeningeal NeoplasmsMeningiomaMutationNeoplasm ProteinsNeurofibromin 2ActinsBromodeoxyuridineCateninsMembrane ProteinsNeoplasm ProteinsNeurofibromin 2RNA, Small Interfering

Identifiers

PMID17962031
PMCPMC2266821
OpenAlexW1978247043

What OpenQuestion holds

Textmetadata
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.