Evidence map›Paper›PMID 21551250›Full record

ArticleCancer research2011

Susceptible stages in Schwann cells for NF1-associated plexiform neurofibroma development.

Lu Q Le, Chiachi Liu, Tracey Shipman, Zhiguo Chen, Ueli Suter, Luis F Parada

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
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  6. Article
  7. TheCancers · 2024
    Review
  8. [Gene therapy strategies and prospects for neurofibromatosis type 1].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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  15. Article
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  17. Article
  18. Article
  19. Insights into the Pathogenesis of NF1-Associated Neoplasms.JID innovations : skin science from molecules to population health · 2021
    Article
  20. Review
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

6 authors at 2 institutions in 2 countries.

Lu Q LeDepartments of Developmental Biology and Dermatology, Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA. Lu.Le@UTSouthwestern.edu
Chiachi Liu
Tracey Shipman
Zhiguo Chen
Ueli Suter
Luis F Parada
ETH Zurich · CHThe University of Texas Southwestern Medical Center · US

Funding

Transgenic CoreP50NS052606 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI CLAPP, DAVID W · 2005 to 2014
$12.6M
NINDS NIH HHS P50 NS052606
6 · The paper itself

Abstract

Stem cells are under strict regulation by both intrinsic factors and the microenvironment. There is increasing evidence that many cancers initiate through acquisition of genetic mutations (loss of intrinsic control) in stem cells or their progenitors, followed by alterations of the surrounding microenvironment (loss of extrinsic control). In neurofibromatosis type 1 (NF1), deregulation of Ras signaling results in development of multiple neurofibromas, complex tumors of the peripheral nerves. Neurofibromas arise from the Schwann cell lineage following loss of function at the NF1 locus, which initiates a cascade of interactions with other cell types in the microenvironment and additional cell autonomous modifications. In this study, we sought to identify whether a temporal "window of opportunity" exists during which cells of the Schwann cell lineage can give rise to neurofibromas following loss of NF1. We showed that acute loss of NF1 in both embryonic and adult Schwann cells can lead to neurofibroma formation. However, the embryonic period when Schwann cell precursors and immature Schwann cells are most abundant coincides with enhanced susceptibility to plexiform neurofibroma tumorigenesis. This model has important implications for understanding early cellular events that dictate neurofibroma development, as well as for the development of novel therapies targeting these tumors.

Indexed as

Genes, Neurofibromatosis 1AnimalsCell Transformation, NeoplasticFemaleGene Expression Regulation, DevelopmentalHyperplasiaIntegrasesMaleMiceMice, Inbred C57BLMice, TransgenicMyelin Proteolipid ProteinNeurofibroma, PlexiformPeripheral NervesPregnancyRecombination, GeneticCre recombinaseIntegrasesMyelin Proteolipid ProteinTamoxifen

Identifiers

PMID21551250
PMCPMC3145496
OpenAlexW2124524275

What OpenQuestion holds

Textmetadata
LicenceTDM
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.