ArticleCancer cell2018
Programming of Schwann Cells by Lats1/2-TAZ/YAP Signaling Drives Malignant Peripheral Nerve Sheath Tumorigenesis.
Article in Cancer cell, 2018. 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
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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.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Survival outcomes of malignant peripheral nerve sheath tumors (MPNSTs) with and without neurofibromatosis type I (NF1): a meta-analysis.World journal of surgical oncology · 2024Pooled it
- LATS kinase activity and tumor suppressor function are regulated by a second autophosphorylation site.The Journal of biological chemistry · 2026Article
- Sox2 protein stability is enhanced by BRafV600E and Pten deletion in adult neural stem/progenitor cells.NPJ precision oncology · 2026Article
- TEAD inhibitors synergize with MEK, SHP2 and mTOR inhibitors in NF1 and NF2 cell lines.microPublication biology · 2026Article
- TEAD inhibitors re-sensitize drug-resistant NF1 MPNST cells to MEK inhibitors.microPublication biology · 2026Article
- Review
- Gallbladder Schwannoma: A Case Report and Literature Review.Diagnostics (Basel, Switzerland) · 2025Article
- Targeting yes-associated protein to overcome imatinib resistance in gastrointestinal stromal tumor drug-tolerant persister cells.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025Article
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- From benign neurofibromas to malignant peripheral nerve sheath tumors (MPNST): a gaming among multiple factors.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Thermal Annealing Enhances Piezoelectricity and Regenerative Potential of PVDF-TrFE Nanofiber Scaffolds.Advanced materials technologies · 2025Article
- The STRIPAK complex is required for radial sorting and laminin receptor expression in Schwann cells.Cell reports · 2025Article
- Discoidin domain receptor inhibitor DDR1-IN-1 induces autophagy and necroptotic cell death in malignant peripheral nerve sheath tumor.Cell death discovery · 2025Article
- YAP Signaling in Glia: Pivotal Roles in Neurological Development, Regeneration and Diseases.Neuroscience bulletin · 2025Review
- Review
- WWC proteins-mediated compensatory mechanism restricts schwannomatosis driven byScience advances · 2025Article
- Schwann cells in regeneration and cancer.Frontiers in pharmacology · 2025Review
- Article
- YAP, TAZ, and Hippo-Dysregulating Fusion Proteins in Cancer.Annual review of cancer biology · 2024Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
Abstract
Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive Schwann cell (SC)-lineage-derived sarcomas. Molecular events driving SC-to-MPNST transformation are incompletely understood. Here, we show that human MPNSTs exhibit elevated HIPPO-TAZ/YAP expression, and that TAZ/YAP hyperactivity in SCs caused by Lats1/2 loss potently induces high-grade nerve-associated tumors with full penetrance. Lats1/2 deficiency reprograms SCs to a cancerous, progenitor-like phenotype and promotes hyperproliferation. Conversely, disruption of TAZ/YAP activity alleviates tumor burden in Lats1/2-deficient mice and inhibits human MPNST cell proliferation. Moreover, genome-wide profiling reveals that TAZ/YAP-TEAD1 directly activates oncogenic programs, including platelet-derived growth factor receptor (PDGFR) signaling. Co-targeting TAZ/YAP and PDGFR pathways inhibits tumor growth. Thus, our findings establish a previously unrecognized convergence between Lats1/2-TAZ/YAP signaling and MPNST pathogenesis, revealing potential therapeutic targets in these untreatable tumors.
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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.