ArticleThe American journal of pathology2010
Nf1-/- Schwann cell-conditioned medium modulates mast cell degranulation by c-Kit-mediated hyperactivation of phosphatidylinositol 3-kinase.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- The Clinical Spectrum of Inflammatory Bowel Disease Associated With Specific Genetic Syndromes: Two Novel Pediatric Cases and a Systematic Review.Frontiers in pediatrics · 2021Pooled it
- Advancing neurofibromatosis research: a comparative review of animal models and their utility in dissecting the tumor microenvironment.Laboratory animal research · 2026Review
- Extracellular vesicles in spine tumors: biological roles, immune modulation, and therapeutic implications.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- Mass spectrometric insights into the protein composition of human cutaneous neurofibromas: comparison of neurofibromas with the overlying skin.British journal of cancer · 2025Article
- Neuronal hyperexcitability drives central and peripheral nervous system tumor progression in models of neurofibromatosis-1.Nature communications · 2022Article
- The roles of GTPase-activating proteins in regulated cell death and tumor immunity.Journal of hematology & oncology · 2021Review
- Release of Mediator Enzyme β-Hexosaminidase and Modulated Gene Expression Accompany Hemocyte Degranulation in Response to Parasitism in the Silkworm Bombyx mori.Biochemical genetics · 2021Article
- AR facilitates YAP-TEAD interaction with the AM promoter to enhance mast cell infiltration into cutaneous neurofibroma.Scientific reports · 2019Article
- Ketotifen Modulates Mast Cell Chemotaxis to Kit-Ligand, but Does Not Impact Mast Cell Numbers, Degranulation, or Tumor Behavior in Neurofibromas ofMolecular cancer therapeutics · 2019Article
- β-Cell Receptor Tyrosine Kinases in Controlling Insulin Secretion and Exocytotic Machinery: c-Kit and Insulin Receptor.Endocrinology · 2018Review
- Contributions of inflammation and tumor microenvironment to neurofibroma tumorigenesis.The Journal of clinical investigation · 2018Article
- KIR2DL5 mutation and loss underlies sporadic dermal neurofibroma pathogenesis and growth.Oncotarget · 2017Article
- The role of the immune system in neurofibromatosis type 1-associated nervous system tumors.CNS oncology · 2017Review
- The role of stem cells in benign tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Contextual signaling in cancer.Seminars in cell & developmental biology · 2016Review
- The new deal: a potential role for secreted vesicles in innate immunity and tumor progression.Frontiers in immunology · 2015Review
- The plexiform neurofibroma microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012Article
- Genetically engineered mouse models shed new light on the pathogenesis of neurofibromatosis type I-related neoplasms of the peripheral nervous system.Brain research bulletin · 2012Review
- Pathogenesis of plexiform neurofibroma: tumor-stromal/hematopoietic interactions in tumor progression.Annual review of pathology · 2012Review
- Kinase suppressor of Ras (KSR1) modulates multiple kit-ligand-dependent mast cell functions.Experimental hematology · 2011Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Neurofibromatosis type 1 (NF1) is a common genetic disorder and is characterized by both malignant and nonmalignant neurofibromas, which are composed of Schwann cells, degranulating mast cells, fibroblasts, and extracellular matrix. We and others have previously shown that hyperactivation of the c-Kit pathway in an Nf1 haploinsufficient microenvironment is required for both tumor formation and progression. Mast cells play a key role in both tumorigenesis and neoangiogenesis via the production of matrix metalloproteinases, heparin, and a range of different growth factors. In the present study, we show that tumorigenic Schwann cells derived from Nf1(-/-) embryos promote increased degranulation of Nf1(+/-) mast cells compared with wild-type mast cells via the secretion of the Kit ligand. Furthermore, we used genetic intercrosses as well as pharmacological agents to link the hyperactivation of the p21(Ras)-phosphatidylinositol 3-kinase (PI3K) pathway to the increased degranulation of Nf1(+/-) mast cells both in vitro and in vivo. These studies identify the p21(Ras)-PI3K pathway as a major regulator of the gain in Nf1(+/-) mast cell degranulation in neurofibromas. Collectively, these studies identify both c-Kit and PI3K as molecular targets that modulate mast cell functions in cases of NF1.
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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.