ReviewGlia2008
How does the Schwann cell lineage form tumors in NF1?
Review in Glia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Care of adults with neurofibromatosis type 1: a clinical practice resource of the American College of Medical Genetics and Genomics (ACMG).Genetics in medicine : official journal of the American College of Medical Genetics · 2018Guideline
- MEK inhibition exhibits efficacy in human and mouse neurofibromatosis tumors.The Journal of clinical investigation · 2013Trial
- Neurofibromatosis Type 1 Presenting With a Mesenteric Plexiform Neurofibroma and Epididymitis.Cureus · 2026Article
- Article
- Mechanical Stiffening Promotes Growth, Invasion, and Mitogen-Activated Protein Kinase Kinase (MEK) Inhibitor Resistance in 3D Plexiform Neurofibroma Cultures.bioRxiv : the preprint server for biology · 2026Article
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- The recurrence and multi-organ involvement of giant penile plexiform neurofibroma in an adult with neurofibromatosis type 1: a case report.BMC urology · 2025Article
- Interferon-Induced Transmembrane Protein 1 (IFITM1) Is Downregulated in Neurofibromatosis Type 1-Associated Malignant Peripheral Nerve Sheath Tumors.International journal of molecular sciences · 2024Article
- Precision oncology in neurofibromatosis type 1: quantification of differential sensitivity to selumetinib in plexiform neurofibromas using single-cell RNA sequencing.Journal of neuro-oncology · 2024Article
- The Lack of Ad Hoc Neuropsychological Assessment in Adults with Neurofibromatosis: A Systematic Review.Journal of clinical medicine · 2024Review
- TheCancers · 2024Review
- A Retrospective Analysis of High Resolution Ultrasound Evaluation of the "Split Fat Sign" in Peripheral Nerve Sheath Tumors.Healthcare (Basel, Switzerland) · 2023Article
- Article
- Neurofibromin Deficiency Causes Epidermal Growth Factor Receptor Upregulation through the Activation of Ras/ERK/SP1 Signaling Pathway in Neurofibromatosis Type 1-Associated Malignant Peripheral Nerve Sheet Tumor.International journal of molecular sciences · 2021Article
- R-Ras subfamily proteins elicit distinct physiologic effects and phosphoproteome alterations in neurofibromin-null MPNST cells.Cell communication and signaling : CCS · 2021Article
- Current progress, challenges and future prospects of indazoles as protein kinase inhibitors for the treatment of cancer.RSC advances · 2021Review
- Natural History and Disease Burden of Neurofibromatosis Type 1 with Plexiform Neurofibromas: A Systematic Literature Review.Adolescent health, medicine and therapeutics · 2021Review
- Identification of a novel PAK1 inhibitor to treat pancreatic cancer.Acta pharmaceutica Sinica. B · 2020Article
- An inducible Cre mouse line to sparsely target nervous system cells, including Remak Schwann cells.Neural development · 2020Article
- Deregulated microRNAs in neurofibromatosis type 1 derived malignant peripheral nerve sheath tumors.Scientific reports · 2020Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Neurofibromas are benign tumors of peripheral nerve that occur sporadically or in patients with the autosomal dominant tumor predisposition syndrome neurofibromatosis type 1 (NF1). Multiple neurofibroma subtypes exist which differ in their site of occurrence, their association with NF1, and their tendency to undergo transformation to become malignant peripheral nerve sheath tumors (MPNSTs), the most common malignancy associated with NF1. Most NF1 patients carry a constitutional mutation of the NF1 tumor suppressor gene. Neurofibromas develop in these patients when an unknown cell type in the Schwann cell lineage loses its remaining functional NF1 gene and initiates a complex series of interactions with other cell types; these interactions may be influenced by aberrant expression of growth factors and growth factor receptors and the action of modifier genes. Cells within certain neurofibroma subtypes subsequently accumulate additional mutations affecting the p19(ARF)-MDM2-TP53 and p16INK4A-Rb signaling cascades, mutations of other as yet unidentified genes, and amplification of growth factor receptor genes, resulting in their transformation into MPNSTs. These observations have been validated using a variety of transgenic and knockout mouse models that recapitulate neurofibroma and MPNST pathogenesis. A new generation of mouse models is also providing important new insights into the identity of the cell type in the Schwann cell lineage that gives rise to neurofibromas. Our improving understanding of the mechanisms underlying the pathogenesis of neurofibromas and MPNSTs raises intriguing new questions about the origin and pathogenesis of these neoplasms and establishes models for the development of new therapies targeting these neoplasms.
Indexed as
Identifiers
What OpenQuestion holds
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.