Evidence map›Paper›PMID 22700876›Full record

ArticleCancer research2012

PTEN and NF1 inactivation in Schwann cells produces a severe phenotype in the peripheral nervous system that promotes the development and malignant progression of peripheral nerve sheath tumors.

Vincent W Keng, Eric P Rahrmann, Adrienne L Watson, Barbara R Tschida, Christopher L Moertel, Walter J Jessen, Tilat A Rizvi, Margaret H Collins, Nancy Ratner, David A Largaespada

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 87 citations in OpenAlex.

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  5. Optogenetic and Endogenous Modulation of CaInternational journal of molecular sciences · 2025
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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

10 authors at 1 institution in 1 country.

Vincent W KengMasonic Cancer Center, Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Eric P Rahrmann
Adrienne L Watson
Barbara R Tschida
Christopher L Moertel
Walter J Jessen
Tilat A Rizvi
Margaret H Collins
Nancy Ratner
David A Largaespada
Cincinnati Children's Hospital Medical Center · US

Funding

TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
Xenograft Core for NF1 Experimental TherapeuticsP50NS057531 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI RATNER, NANCY · 2008 to 2012
$6.8M
Minnesota Training Program in VirologyT32AI083196 · NIAID · UNIVERSITY OF MINNESOTA · PI Louis M Mansky · 2010 to 2026
$3.2M
NF1 GENE IN MYELOID LEUKEMIA AND CYTOKINE SIGNALINGR29CA078269 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LARGAESPADA, DAVID ANDREW · 1998 to 2002
$293k
NCI NIH HHS R29 CA078269NCI NIH HHS T32 CA009138NIAID NIH HHS T32 AI083196NINDS NIH HHS P50 NS057531PHS HHS P50 N5057531
6 · The paper itself

Abstract

The genetic evolution from a benign neurofibroma to a malignant sarcoma in patients with neurofibromatosis type 1 (NF1) syndrome remains unclear. Schwann cells and/or their precursor cells are believed to be the primary pathogenic cell in neurofibromas because they harbor biallelic neurofibromin 1 (NF1) gene mutations. However, the phosphatase and tensin homolog (Pten) and neurofibromatosis 1 (Nf1) genes recently were found to be comutated in high-grade peripheral nerve sheath tumors (PNST) in mice. In this study, we created transgenic mice that lack both Pten and Nf1 in Schwann cells and Schwann cell precursor cells to validate the role of these two genes in PNST formation in vivo. Haploinsufficiency or complete loss of Pten dramatically accelerated neurofibroma development and led to the development of higher grade PNSTs in the context of Nf1 loss. Pten dosage, together with Nf1 loss, was sufficient for the progression from low-grade to high-grade PNSTs. Genetic analysis of human malignant PNSTs (MPNST) also revealed downregulation of PTEN expression, suggesting that Pten-regulated pathways are major tumor-suppressive barriers to neurofibroma progression. Together, our findings establish a novel mouse model that can rapidly recapitulate the onset of human neurofibroma tumorigenesis and the progression to MPNSTs.

Indexed as

AnimalsDisease ProgressionHumansMiceMice, TransgenicNerve Sheath NeoplasmsNeurofibromin 1OligopeptidesPeripheral Nervous SystemPhenotypePTEN PhosphohydrolaseSchwann CellsNeurofibromin 1OligopeptidesPTEN PhosphohydrolasePTEN protein, humantryptophyl-tryptophyl-tryptophyl-prolyl-phenylalanyl-arginyl-arginine

Identifiers

PMID22700876
PMCPMC3428071
OpenAlexW2013915588

What OpenQuestion holds

Textmetadata
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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.