Evidence map›Paper›PMID 22160322›Full record

ReviewActa neuropathologica2012

Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms.

Steven L Carroll

Abstract readReview
In one paragraph

Review in Acta neuropathologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing 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

68 citing papers in PubMed, 120 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. The interaction between oxidative stress and Schwann cells.Experimental biology and medicine (Maywood, N.J.) · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Schwann cells in regeneration and cancer.Frontiers in pharmacology · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Co-Existing Ectopic Cortisol-Producing Adenoma and Retroperitoneal Schwannoma, a Rare Case Report.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

8 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

1 author at 1 institution in 1 country.

Steven L CarrollDivision of Neuropathology, Department of Pathology, University of Alabama at Birmingham, 1720 Seventh Avenue South, SC930G3, Birmingham, AL 35294-0017, USA. scarroll@uab.edu
University of Alabama at Birmingham · US

Funding

Alabama Neuroscience Blueprint Core CenterP30NS057098 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROTH, KEVIN A · 2006 to 2010
$9.5M
Novel Treatment of NF-1 Associated Malignant Peripheral Nerve Sheath TumorsR01CA122804 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARROLL, STEVEN L. · 2008 to 2012
$1.5M
Role of Neuregulin-1 in Schwann Cell NeoplasiaR01NS048353 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARROLL, STEVEN L. · 2004 to 2008
$1.3M
Multi-Modal Lysosomotropic Death Therapy for Malignant Peripheral Nerve Sheath TuR01CA134773 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROTH, KEVIN A · 2009 to 2011
$722k
NCI NIH HHS R01 CA122804NCI NIH HHS R01 CA134773NINDS NIH HHS P30 NS057098NINDS NIH HHS P30 NS57098NINDS NIH HHS R01 NS048353
6 · The paper itself

Abstract

Neurofibromas, schwannomas and malignant peripheral nerve sheath tumors (MPNSTs) all arise from the Schwann cell lineage. Despite their common origin, these tumor types have distinct pathologies and clinical behaviors; a growing body of evidence indicates that they also arise via distinct pathogenic mechanisms. Identification of the genes that are mutated in genetic diseases characterized by the development of either neurofibromas and MPNSTs [neurofibromatosis type 1 (NF1)] or schwannomas [neurofibromatosis type 2 (NF2), schwannomatosis and Carney complex type 1] has greatly advanced our understanding of these mechanisms. The development of genetically engineered mice with ablation of NF1, NF2, SMARCB1/INI1 or PRKAR1A has confirmed the key role these genes play in peripheral nerve sheath tumorigenesis. Establishing the functions of the NF1, NF2, SMARCB1/INI1 and PRKAR1A gene products has led to the identification of key cytoplasmic signaling pathways promoting Schwann cell neoplasia and identified new therapeutic targets. Analyses of human neoplasms and genetically engineered mouse models have established that interactions with other tumor suppressors such as TP53 and CDKN2A promote neurofibroma-MPNST progression and indicate that intratumoral interactions between neoplastic and non-neoplastic cell types play an essential role in peripheral nerve sheath tumorigenesis. Recent advances have also provided new insights into the identity of the neural crest-derived populations that give rise to different types of peripheral nerve sheath tumors. Based on these findings, we now have an initial outline of the molecular mechanisms driving the pathogenesis of neurofibromas, MPNSTs and schwannomas. However, this improved understanding in turn raises a host of intriguing new questions.

Indexed as

Cell Transformation, NeoplasticHumansNerve Sheath NeoplasmsNeurilemmomaNeurofibromatosesSchwann Cells

Identifiers

PMID22160322
PMCPMC3288530
OpenAlexW2060362092

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.