ArticleOncogene2008
c-Myc and beta-catenin cooperate with loss of p53 to generate multiple members of the primitive neuroectodermal tumor family in mice.
Article in Oncogene, 2008. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Construction of tumor organoids and their application to cancer research and therapy.Theranostics · 2024Review
- Applications of organoid technology to brain tumors.CNS neuroscience & therapeutics · 2023Review
- Glioblastoma modeling with 3D organoids: progress and challenges.Oxford open neuroscience · 2023Review
- Human pluripotent stem cell-derived brain organoids as in vitro models for studying neural disorders and cancer.Cell & bioscience · 2021Review
- Down-regulation of 14-3-3zeta reduces proliferation and increases apoptosis in human glioblastoma.Cancer gene therapy · 2020Article
- Author Correction: Genetically engineered cerebral organoids model brain tumor formation.Nature methods · 2018Article
- Genetically engineered cerebral organoids model brain tumor formation.Nature methods · 2018Article
- Plk1 Inhibition Enhances the Efficacy of BET Epigenetic Reader Blockade in Castration-Resistant Prostate Cancer.Molecular cancer therapeutics · 2018Article
- BAI1 Suppresses Medulloblastoma Formation by Protecting p53 from Mdm2-Mediated Degradation.Cancer cell · 2018Article
- Mice Expressing Myc in Neural Precursors Develop Choroid Plexus and Ciliary Body Tumors.The American journal of pathology · 2018Article
- Article
- A new genetically engineered mouse model of choroid plexus carcinoma.Biochemical and biophysical research communications · 2018Article
- Somatic cell transfer of c-Myc and Bcl-2 induces large-cell anaplastic medulloblastomas in mice.Journal of neuro-oncology · 2016Article
- Wnt activation affects proliferation, invasiveness and radiosensitivity in medulloblastoma.Journal of neuro-oncology · 2015Article
- Signals that regulate the oncogenic fate of neural stem cells and progenitors.Experimental neurology · 2014Review
- The prenatal origins of cancer.Nature reviews. Cancer · 2014Review
- Adult primitive neuroectodermal tumors: the prognostic value of supratentorial location.Journal of neuro-oncology · 2013Article
- What underlies the diversity of brain tumors?Cancer metastasis reviews · 2013Review
- The role of the WNT/β-catenin pathway in central nervous system primitive neuroectodermal tumours (CNS PNETs).British journal of cancer · 2013Article
- WNT/β-catenin pathway activation in Myc immortalised cerebellar progenitor cells inhibits neuronal differentiation and generates tumours resembling medulloblastoma.British journal of cancer · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Primitive neuroectodermal tumors (PNETs) are a family of primary malignant brain tumors that include medulloblastomas. Although genetic models of a subset of medulloblastomas are documented over the past decade, the molecular basis of other subclasses of PNET remains unclear. As elevated c-Myc expression, activation of Wnt/beta-catenin signaling and dysfunction of p53 are seen in human PNETs, we investigated what role these abnormalities have in the formation of PNETs. Incorporating these abnormalities, we generated supratentorial PNET (sPNET) in mice using somatic cell gene transfer. We show that sPNETs arise from GFAP-expressing cells by forced c-Myc expression combined with p53 inactivation. beta-catenin activation promotes tumor progression and induces divergent differentiation. These c-Myc+beta-catenin-induced PNETs are histologically similar to large cell/anaplastic medulloblastomas and can occur in both cerebrum and cerebellum. Furthermore, we have obtained one PNET with marked epithelial differentiation having histological resemblance to choroid plexus carcinoma in this series. Our results in mice suggest that sPNET with varied differentiation and large cell/anaplastic medulloblastomas may be two tumor groups with similar genetic foundations. These data provide insights into the biology and classification of human PNETs and suggest that multiple tumor types or variants can be generated from a fixed set of genetic abnormalities.
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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.