ArticleOncotarget2016
Spatially- and temporally-controlled postnatal p53 knockdown cooperates with embryonic Schwann cell precursor Nf1 gene loss to promote malignant peripheral nerve sheath tumor formation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- UBR5 in Tumor Biology: Exploring Mechanisms of Immune Regulation and Possible Therapeutic Implications in MPNST.Cancers · 2025Review
- Malignant Peripheral Nerve Sheath Tumor, a Heterogeneous, Aggressive Cancer with Diverse Biomarkers and No Targeted Standard of Care: Review of the Literature and Ongoing Investigational Agents.Targeted oncology · 2024Review
- Article
- Discrepancies in indel software resolution with somatic CRISPR/Cas9 tumorigenesis models.Scientific reports · 2023Article
- Malignant Peripheral Nerve Sheath Tumors: Latest Concepts in Disease Pathogenesis and Clinical Management.Cancers · 2023Review
- Neurofibroma Development in Neurofibromatosis Type 1: Insights from Cellular Origin and Schwann Cell Lineage Development.Cancers · 2022Review
- Review
- Enhancer reprogramming in PRC2-deficient malignant peripheral nerve sheath tumors induces a targetable de-differentiated state.Acta neuropathologica · 2021Article
- Toward Understanding the Mechanisms of Malignant Peripheral Nerve Sheath Tumor Development.International journal of molecular sciences · 2021Review
- Stem-like cells drive NF1-associated MPNST functional heterogeneity and tumor progression.Cell stem cell · 2021Article
- Pharmacological Approaches in Neurofibromatosis Type 1-Associated Nervous System Tumors.Cancers · 2021Review
- Chromosome 8 gain is associated with high-grade transformation in MPNST.JCI insight · 2021Article
- Humanized neurofibroma model from induced pluripotent stem cells delineates tumor pathogenesis and developmental origins.The Journal of clinical investigation · 2021Article
- Diagnosis and management of malignant peripheral nerve sheath tumors: Current practice and future perspectives.Neuro-oncology advances · 2020Review
- Whole exome sequencing reveals the maintained polyclonal nature from primary to metastatic malignant peripheral nerve sheath tumor in two patients with NF1.Neuro-oncology advances · 2020Article
- Translating current basic research into future therapies for neurofibromatosis type 1.British journal of cancer · 2020Review
- Understanding a complicated Gal-1.Neuro-oncology · 2019Article
- Heterozygous Tumor Suppressor Microenvironment in Cancer Development.Trends in cancer · 2019Review
- Neurofibromin 1 expression is negatively correlated with malignancy and prognosis of epithelial ovarian cancer.International journal of clinical and experimental pathology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive sarcomas that arise sporadically or in association with the Neurofibromatosis type 1 (NF1) cancer predisposition syndrome. In individuals with NF1, MPNSTs are hypothesized to arise from Nf1-deficient Schwann cell precursor cells following the somatic acquisition of secondary cooperating genetic mutations (e.g., p53 loss). To model this sequential genetic cooperativity, we coupled somatic lentivirus-mediated p53 knockdown in the adult right sciatic nerve with embryonic Schwann cell precursor Nf1 gene inactivation in two different Nf1 conditional knockout mouse strains. Using this approach, ~60% of mice with Periostin-Cre-mediated Nf1 gene inactivation (Periostin-Cre; Nf1(flox/flox) mice) developed tumors classified as low-grade MPNSTs following p53 knockdown (mean, 6 months). Similarly, ~70% of Nf1+/- mice with GFAP-Cre-mediated Nf1 gene inactivation (GFAP-Cre; Nf1(flox/null) mice) developed low-grade MPNSTs following p53 knockdown (mean, 3 months). In addition, wild-type and Nf1+/- mice with GFAP-Cre-mediated Nf1 loss develop MPNSTs following somatic p53 knockout with different latencies, suggesting potential influences of Nf1+/- stromal cells in MPNST pathogenesis. Collectively, this new MPNST model system permits the analysis of somatically-acquired events as well as tumor microenvironment signals that potentially cooperate with Nf1 loss in the development and progression of this deadly malignancy.
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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.