ArticleNeoplasia (New York, N.Y.)2014
Neurogenin 3-directed cre deletion of Tsc1 gene causes pancreatic acinar carcinoma.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- KRT13 Drives Pancreatic Cancer Malignancy Via the PI3K/AKT-PPARG Axis While Enhancing Sensitivity to Navitoclax.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Derivation of pancreatic acinar cell carcinoma cell line HS-1 as a patient-derived tumor organoid.Cancer science · 2023Article
- An aberrant DNA methylation signature for predicting the prognosis of head and neck squamous cell carcinoma.Cancer medicine · 2021Article
- Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021Review
- Prognostic value and immunological characteristics of a novel autophagy-related signature in pancreatic cancer.Journal of biosciences · 2021Article
- Pax4 synergistically acts with Pdx1, Ngn3 and MafA to induce HuMSCs to differentiate into functional pancreatic β-cells.Experimental and therapeutic medicine · 2019Article
- Prevention of pancreatic acinar cell carcinoma by Roux-en-Y Gastric Bypass Surgery.Nature communications · 2018Article
- Article
- Novel patient-derived xenograft mouse model for pancreatic acinar cell carcinoma demonstrates single agent activity of oxaliplatin.Journal of translational medicine · 2016Article
- Pancreas-specific activation of mTOR and loss of p53 induce tumors reminiscent of acinar cell carcinoma.Molecular cancer · 2015Article
- Intestinal mTOR regulates GLP-1 production in mouse L cells.Diabetologia · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of tuberous sclerosis complex (TSC) in the pathogenesis of pancreatic cancers remains largely unknown. The present study shows that neurogenin 3 directed Cre deletion of Tsc1 gene induces the development of pancreatic acinar carcinoma. By cross-breeding the Neurog3-cre mice with Tsc1 (loxp/loxp) mice, we generated the Neurog3-Tsc1-/- transgenic mice in which Tsc1 gene is deleted and mTOR signaling activated in the pancreatic progenitor cells. All Neurog3-Tsc1-/- mice developed notable adenocarcinoma-like lesions in pancreas starting from the age of 100 days old. The tumor lesions are composed of cells with morphological and molecular resemblance to acinar cells. Metastasis of neoplasm to liver and lung was detected in 5% of animals. Inhibition of mTOR signaling by rapamycin significantly attenuated the growth of the neoplasm. Relapse of the neoplasm occurred within 14 days upon cessation of rapamycin treatment. Our studies indicate that activation of mTOR signaling in the pancreatic progenitor cells may trigger the development of acinar carcinoma. Thus, mTOR may serve as a potential target for treatment of pancreatic acinar carcinoma.
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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.