ArticleOncotarget2016
Characterization of pancreatic glucagon-producing tumors and pituitary gland tumors in transgenic mice overexpressing MYCN in hGFAP-positive cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Targeting the MYCN-MDM2 pathways for cancer therapy: Are they druggable?Genes & diseases · 2025Review
- N-MYC regulates cell survival via eIF4G1 in inv(16) acute myeloid leukemia.Science advances · 2024Article
- Mouse models of pediatric high-grade gliomas with MYCN amplification reveal intratumoral heterogeneity and lineage signatures.Nature communications · 2023Article
- Article
- The tumor suppressor CREBBP and the oncogene MYCN cooperate to induce malignant brain tumors in mice.Oncogenesis · 2023Article
- The remission phase in adolescents and young adults with newly diagnosed type 1 diabetes mellitus: prevalence, predicting factors and glycemic control during follow-up.Archives of endocrinology and metabolism · 2022Article
- The OncogeneCancers · 2021Article
- Simultaneous Brg1 Knockout and MYCN Overexpression in Cerebellar Granule Neuron Precursors Is Insufficient to Drive Tumor Formation but Temporarily Enhances their Proliferation and Delays their Migration.Cerebellum (London, England) · 2021Article
- LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis.Cancer cell international · 2021Article
- Time series modeling of cell cycle exit identifies Brd4 dependent regulation of cerebellar neurogenesis.Nature communications · 2019Article
- N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer.The Journal of clinical investigation · 2019Article
- Prolactin - a pleiotropic factor in health and disease.Nature reviews. Endocrinology · 2019Review
- Insights into the biology and treatment strategies of pancreatic neuroendocrine tumors.Annals of pancreatic cancer · 2019Article
- Molecular characterization of metastatic pancreatic neuroendocrine tumors (PNETs) using whole-genome and transcriptome sequencing.Cold Spring Harbor molecular case studies · 2018Article
- Natural and molecular history of prolactinoma: insights from aOncotarget · 2018Article
- MYCN-mediated murine cancer models.Aging · 2017Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amplification or overexpression of MYCN is involved in development and maintenance of multiple malignancies. A subset of these tumors originates from neural precursors, including the most aggressive forms of the childhood tumors, neuroblastoma and medulloblastoma. In order to model the spectrum of MYCN-driven neoplasms in mice, we transgenically overexpressed MYCN under the control of the human GFAP-promoter that, among other targets, drives expression in neural progenitor cells. However, LSL-MYCN;hGFAP-Cre double transgenic mice did neither develop neural crest tumors nor tumors of the central nervous system, but presented with neuroendocrine tumors of the pancreas and, less frequently, the pituitary gland. Pituitary tumors expressed chromogranin A and closely resembled human pituitary adenomas. Pancreatic tumors strongly produced and secreted glucagon, suggesting that they derived from glucagon- and GFAP-positive islet cells. Interestingly, 3 out of 9 human pancreatic neuroendocrine tumors expressed MYCN, supporting the similarity of the mouse tumors to the human system. Serial transplantations of mouse tumor cells into immunocompromised mice confirmed their fully transformed phenotype. MYCN-directed treatment by AuroraA- or Brd4-inhibitors resulted in significantly decreased cell proliferation in vitro and reduced tumor growth in vivo. In summary, we provide a novel mouse model for neuroendocrine tumors of the pancreas and pituitary gland that is dependent on MYCN expression and that may help to evaluate MYCN-directed therapies.
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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.