ArticleScientific reports2024
Combined deletion of MEN1, ATRX and PTEN triggers development of high-grade pancreatic neuroendocrine tumors in mice.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Clinicopathological and molecular determinants of pancreatic neuroendocrine tumors: toward precision risk stratification.Journal of translational medicine · 2026Review
- Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms.Molecular cancer · 2026Article
- Validation of WHO 2017 Classification and Identification of Prognostic Factors in Patients with Pancreatic Neuroendocrine Neoplasms: A Real-World Experience in Taiwan.Journal of Cancer · 2025Article
- Article
- Molecular Basis of Pancreatic Neuroendocrine Tumors.International journal of molecular sciences · 2024Review
- Menin in Cancer.Genes · 2024Review
- Mutant ATRX: pathogenesis of ATRX syndrome and cancer.Frontiers in molecular biosciences · 2024Review
- NET Models Meeting 2024 white paper: the current state of neuroendocrine tumour research models and our future aspirations.Endocrine oncology (Bristol, England) · 2024Review
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Pancreatic neuroendocrine tumors (PanNETs) are a heterogeneous group of tumors that exhibit an unpredictable and broad spectrum of clinical presentations and biological aggressiveness. Surgical resection is still the only curative therapeutic option for localized PanNET, but the majority of patients are diagnosed at an advanced and metastatic stage with limited therapeutic options. Key factors limiting the development of new therapeutics are the extensive heterogeneity of PanNETs and the lack of appropriate clinically relevant models. In that context, genomic sequencing of human PanNETs revealed recurrent mutations and structural alterations in several tumor suppressors. Here, we demonstrated that combined loss of MEN1, ATRX, and PTEN, tumor suppressors commonly mutated in human PanNETs, triggers the development of high-grade pancreatic neuroendocrine tumors in mice. Histopathological evaluation and gene expression analyses of the developed tumors confirm the presence of PanNET hallmarks and significant overlap in gene expression patterns found in human disease. Thus, we postulate that the presented novel genetically defined mouse model is the first clinically relevant immunocompetent high-grade PanNET mouse model.
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