Evidence map›Paper›PMID 26190195›Full record

ArticleHuman pathology2015

Clinicopathologic implications of NF1 gene alterations in diffuse gliomas.

M Adelita Vizcaíno, Smit Shah, Charles G Eberhart, Fausto J Rodriguez

Abstract read
In one paragraph

Article in Human pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
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  4. The molecular landscape of glioblastoma-associated epilepsy.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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  12. Annals of translational medicine · 2021
    Article
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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

4 authors at 4 institutions in 2 countries.

M Adelita VizcaínoDepartment of Cellular and Tissue Biology, Faculty of Medicine, UNAM, Mexico City, Mexico 06010; Division of Neuropathology, Johns Hopkins University School of Medicine, 1800 Orleans Street, Baltimore, MD 21231.
Smit ShahDivision of Neuropathology, Johns Hopkins University School of Medicine, 1800 Orleans Street, Baltimore, MD 21231; Rutgers Robert Wood Johnson Medical School in New Jersey, 125 Paterson Street, New Brunswick, NJ 08901.
Charles G EberhartDivision of Neuropathology, Johns Hopkins University School of Medicine, 1800 Orleans Street, Baltimore, MD 21231; Sydney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, 1800 Orleans Street, Baltimore, MD 21231.
Fausto J RodriguezDivision of Neuropathology, Johns Hopkins University School of Medicine, 1800 Orleans Street, Baltimore, MD 21231; Sydney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, 1800 Orleans Street, Baltimore, MD 21231. Electronic address: frodrig4@jhmi.edu.
Johns Hopkins University · USJohnson University · USSidney Kimmel Comprehensive Cancer Center · USUniversidad Nacional Autónoma de México · MX

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

Recent studies have identified somatic alterations in the gene encoding for neurofibromin (NF1) in a subset of glioblastoma (GBM), usually associated with the mesenchymal molecular subtype. To understand the significance of NF1 genetic alterations in diffuse gliomas in general, we evaluated public databases and tested for NF1 copy number alterations in a cohort using fluorescence in situ hybridization. NF1 genetic loss (homozygous NF1 deletions or mutations with predicted functional consequences) was present in 30 (of 281) (11%) GBM and 21 (of 286) (7%) lower-grade gliomas in The Cancer Genome Atlas data. Furthermore, NF1 loss was associated with worse overall and disease-specific survival in the lower-grade glioma, but not GBM, Group in The Cancer Genome Atlas cohort. IDH1 or 2 mutations co-existed in lower-grade gliomas with NF1 loss (36%) but not in GBM. In our cohort studied by fluorescence in situ hybridization, NF1/17q (n = 2) or whole Ch17 (n = 3) losses were only identified in the GBM group (5/86 [6%]). Tumors with NF1/Ch17 loss were predominantly adult GBM (4/5); lacked EGFR amplification (0/4), strong p53 immunolabeling (1/5), or IDH1 (R132H) protein expression (0/5); but expressed the mesenchymal marker podoplanin in 4/5. NF1 genetic loss occurs in a subset of diffuse gliomas, and its significance deserves further exploration.

Indexed as

Biomarkers, TumorBrain NeoplasmsGene DeletionGene DosageGenetic Predisposition to DiseaseGliomaHomozygoteHumansIn Situ Hybridization, FluorescenceKaplan-Meier EstimateMutationNeoplasm GradingNeurofibromin 1PhenotypeTime FactorsBiomarkers, TumorNeurofibromin 1FISHGlioblastomaGliomaNeurofibromatosisNeurofibrominNF1

Identifiers

PMID26190195
PMCPMC4703095
OpenAlexW2096295435

What OpenQuestion holds

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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.