Evidence map›Paper›PMID 24509877›Full record

ArticleOncogene2014

MAF mediates crosstalk between Ras-MAPK and mTOR signaling in NF1.

M E Brundage, P Tandon, D W Eaves, J P Williams, S J Miller, R H Hennigan, A Jegga, T P Cripe, N Ratner

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  15. Article
  16. Loss of function of NF1 is a mechanism of acquired resistance to endocrine therapy in lobular breast cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2019
    Article
  17. Article
  18. Involvement of Aryl hydrocarbon receptor in myelination and in human nerve sheath tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. 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

9 authors at 3 institutions in 1 country.

M E BrundageDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
P TandonDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
D W EavesDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
J P WilliamsDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
S J MillerDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
R H HenniganDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
A JeggaDivision Biomedical Informatics, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID 0000000248817752
T P Cripe1] Division of Oncology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA [2] Division of Hematology/Oncology/BMT, Nationwide Children's Hospital, The Ohio State University, Columbus, OH, USA.
N RatnerDivision of Experimental Hematology and Cancer Biology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USNationwide Children's Hospital · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
MITOGENIC ACTIVITIES IN NEUROFIBROMATOSISR01NS028840 · NINDS · UNIVERSITY OF CINCINNATI · PI NANCY RATNER · 1990 to 2026
$10.1M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI THOMPSON, SUSAN D · 2001 to 2015
$9.2M
Xenograft Core for NF1 Experimental TherapeuticsP50NS057531 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI RIZVI, TILAT · 2008 to 2012
$6.8M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
TRAINING IN DEVELOPMENTAL AND PERINATAL ENDOCRINOLOGYT32HD007463 · NICHD · CINCINNATI CHILDRENS HOSP MED CTR · PI HANDWERGER, STUART · 1994 to 2010
$1.5M
Characterizing the role of specific Ras proteins in neurofibroma and MPNST formatF32NS083249 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI TANDON, PREETI · 2013 to 2014
$102k
NCI NIH HHS T32 CA117846NIAMS NIH HHS AR-47363NIAMS NIH HHS P30 AR047363NICHD NIH HHS T32 HD007463NICHD NIH HHS T32HD07463NIDDK NIH HHS DK78392NIDDK NIH HHS DK90971NIDDK NIH HHS P30 DK078392NIDDK NIH HHS P30 DK090971NINDS NIH HHS F32 NS083249NINDS NIH HHS NIH-P50-NS057531NINDS NIH HHS P50 NS057531NINDS NIH HHS R01 NS028840
6 · The paper itself

Abstract

Mutations in the neurofibromatosis type 1 (NF1) tumor suppressor gene are common in cancer and can cause resistance to therapy. Using transcriptome analysis we identified MAF as an NF1- regulated transcription factor and verified MAF regulation through RAS/MAPK/AP-1 signaling in malignant peripheral nerve sheath tumor (MPNST) cell lines. MAF was also downregulated in human MPNST. Acute re-expression of MAF promoted expression of glial differentiation markers in MPNST cells in vitro, decreased self-renewal of embryonic precursors and transiently affected tumor cell phenotypes in vitro by increasing MPNST cell death and reducing metabolic activity and anchorage-independent growth. Paradoxically, chronic MAF overexpression enhanced MPNST cell tumor growth in vivo, correlating with elevated pS6 in vitro and in vivo. RAD001 blocked MAF-mediated tumor growth, and MAF regulated the mTOR pathway through DEPTOR. MAPK inhibition with NF1 loss of function is predicted to show limited efficacy due to reactivation of mTOR signaling via MAF.

Indexed as

MAP Kinase Signaling SystemAnimalsCell DifferentiationDown-RegulationFemaleGene Expression Regulation, NeoplasticGenes, Neurofibromatosis 1HumansMiceMice, NudeNeoplasm TransplantationNerve Sheath NeoplasmsNeurofibromatosis 1Neurofibromin 1NeurogliaOligonucleotide Array Sequence AnalysisMAF protein, humanMTOR protein, humanNeurofibromin 1Proto-Oncogene Proteins c-mafras ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID24509877
PMCPMC4127377
OpenAlexW2050825930

What OpenQuestion holds

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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.