Evidence map›Paper›PMID 22492957›Full record

ArticleNeuro-oncology2012

Interplay among BRAF, p16, p53, and MIB1 in pediatric low-grade gliomas.

Craig Horbinski, Marina N Nikiforova, Jill M Hagenkord, Ronald L Hamilton, Ian F Pollack

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Role of surgery in the treatment of pediatric low-grade glioma with various degrees of brain stem involvement.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
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  4. Review
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  11. Article
  12. ITGB3BP is a potential biomarker associated with poor prognosis of glioma.Journal of cellular and molecular medicine · 2022
    Article
  13. Review
  14. Review
  15. Review
  16. Article
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  18. Article
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15 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 1 country.

Craig HorbinskiDepartment of Pathology, University of Kentucky, MS-155, 800 Rose Street, Lexington, KY 40536, USA. craig.horbinski@uky.edu
Marina N Nikiforova
Jill M Hagenkord
Ronald L Hamilton
Ian F Pollack
University of Kentucky · USChildren's Hospital of Pittsburgh · USComplete Genomics (United States) · USUniversity of Pittsburgh · US

Funding

MOLECULAR MARKERS AS PREDICTORS OF OUTCOME IN GLIOMASR01NS037704 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI POLLACK, IAN F. · 1998 to 2015
$4.5M
The Significance of Isocitrate Dehydrogenase Mutations in GliomasK08CA155764 · NCI · UNIVERSITY OF KENTUCKY · PI HORBINSKI, CRAIG MICHAEL · 2011 to 2015
$857k
NCI NIH HHS K08 CA155764NCI NIH HHS K08 CA155764-01A1NINDS NIH HHS R01NS37704
6 · The paper itself

Abstract

BRAF rearrangements and BRAF V600E point mutations are recurring events in pediatric low-grade gliomas. However, their clinical significance, including possible interactions between these markers and other glioma biomarkers, is unclear. In this study a retrospective cohort of 198 pediatric low-grade gliomas (including 40 treated with adjuvant therapy) was analyzed for BRAF rearrangements, BRAF V600E, p16/CDKN2A deletion, p53 expression, and MIB1 proliferation index. In tumors with BRAF rearrangement, homozygous p16 deletion correlated with shorter progression-free survival (P = .04). A high MIB1 proliferation index trended toward worse response to adjuvant radiotherapy compared to BRAF-rearranged, p16-intact tumors (P = .08). On multivariate analysis, the 2 most consistently powerful independent adverse prognostic markers were midline location (P = .0001) and p16 deletion (P = .03). Tumors with BRAF V600E had a strong trend toward an increased risk for progression (hazard ratio = 2.48, P = .07), whereas those with BRAF rearrangement had a milder trend toward reduced risk (hazard ratio = .54, P = .15). These data suggest that p16 deletion adversely impacts the outcomes of BRAF-driven gliomas, that high proliferation index may be a better marker of progression risk than BRAF, that BRAF rearrangement and BRAF V600E might not necessarily produce comparable outcomes, and that none of these markers is stronger than tumor location in determining prognosis in pediatric low-grade gliomas.

Indexed as

AdolescentAdultBrain NeoplasmsChildChild, PreschoolCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmFemaleFollow-Up StudiesGene DeletionGene RearrangementGliomaHumansInfantInfant, NewbornIn Situ Hybridization, FluorescenceBRAF protein, humanCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmMIB1 ligase, humanNeoplasm ProteinsProto-Oncogene Proteins B-rafTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID22492957
PMCPMC3367847
OpenAlexW2129554457

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.