Evidence map›Paper›PMID 22159586›Full record

ReviewCellular and molecular life sciences : CMLS2012

MAPK pathway activation in pilocytic astrocytoma.

David T W Jones, Jan Gronych, Peter Lichter, Olaf Witt, Stefan M Pfister

Registry-linked trialAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06666348 (A Phase 1/2 Study of Mirdametinib and Vinblastine for Newly Diagnosed or Previously Untreated Patients With Pediatric Low-grade Glioma and Activation of the MAPK Pathway), which is not on this map. Cited by 114 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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.

NCT06666348 phase1 / phase2recruitingnot on this mapstarted 2026, after this paper: background citation

A Phase 1/2 Study of Mirdametinib and Vinblastine for Newly Diagnosed or Previously Untreated Patients With Pediatric Low-grade Glioma and Activation of the MAPK Pathway

TypeinterventionalSponsorSt. Justine's HospitalRan2026 to 2033Enrolled50ConditionsPediatric Low-grade GliomaArmsMirdametinib
3 · Its place in the literature

Who cites it

114 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Prognostic factors in diffuse leptomeningeal glioneuronal tumor (DLGNT): a systematic review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2022
    Pooled it
  2. Pooled it
  3. Trial
  4. Systems biology-driven drug repurposing in glioblastomaResearch in pharmaceutical sciences · 2026
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  16. MOST wanted: navigating the MAPK-OIS-SASP-tumor microenvironment axis in primary pediatric low-grade glioma and preclinical models.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  17. Molecular-targeted therapy for childhood low-grade glial and glioneuronal tumors.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  18. Review
  19. Canadian Consensus for Treatment of BRAFCurrent oncology (Toronto, Ont.) · 2024
    Article
  20. Article

54 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.

David T W JonesDivision of Molecular Genetics, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120, Heidelberg, Germany.
Jan Gronych
Peter Lichter
Olaf Witt
Stefan M Pfister

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pilocytic astrocytoma (PA) is the most common tumor of the pediatric central nervous system (CNS). A body of research over recent years has demonstrated a key role for mitogen-activated protein kinase (MAPK) pathway signaling in the development and behavior of PAs. Several mechanisms lead to activation of this pathway in PA, mostly in a mutually exclusive manner, with constitutive BRAF kinase activation subsequent to gene fusion being the most frequent. The high specificity of this fusion to PA when compared with other CNS tumors has diagnostic utility. In addition, the frequency of alteration of this key pathway provides an opportunity for molecularly targeted therapy in this tumor. Here, we review the current knowledge on mechanisms of MAPK activation in PA and some of the downstream consequences of this activation, which are now starting to be elucidated both in vitro and in vivo, as well as clinical considerations and possible future directions.

Indexed as

MAP Kinase Signaling SystemAnimalsAstrocytomaDisease Models, AnimalGene FusionHumansMiceModels, GeneticNeurofibromin 1Proto-Oncogene Proteins B-rafNeurofibromin 1Proto-Oncogene Proteins B-raf

Identifiers

PMID22159586
PMCPMC3350769

What OpenQuestion holds

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Registered trials

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.