ArticleOncogene2016
p53 mutations cooperate with oncogenic Kras to promote adenocarcinoma from pancreatic ductal cells.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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.
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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
94 citing papers in PubMed, 156 citations in OpenAlex.
- Review
- Dietary Fat Content Influences PanIN Progression and Pancreatic Cancer Development in Mice.Cancer research communications · 2026Article
- Article
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Dietary Fat Content Influences PanIN Progression and Pancreatic Cancer Development in Mice.bioRxiv : the preprint server for biology · 2025Article
- Molecular characterization and prognostic implications of KRAS mutations in pancreatic cancer patients: insights from multi-cohort analysis.NPJ precision oncology · 2025Article
- Early neoplastic lesions of the pancreas: initiation, progression, and opportunities for precancer interception.The Journal of clinical investigation · 2025Review
- DNA Origami-Cyanine Nanocomplex for Precision Imaging of KRAS-Mutant Pancreatic Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Integrated Stress Response in Pancreatic Development, Tissue Homeostasis, and Cancer.Gastroenterology · 2024Review
- Extracellular Matrix Cues Regulate Mechanosensing and Mechanotransduction of Cancer Cells.Cells · 2024Review
- Identification and analysis of pancreatic intraepithelial neoplasia: opportunities and challenges.Frontiers in endocrinology · 2024Review
- Senescence program and its reprogramming in pancreatic premalignancy.Cell death & disease · 2023Review
- Intrapancreatic fat, pancreatitis, and pancreatic cancer.Cellular and molecular life sciences : CMLS · 2023Review
- Analysis of Donor Pancreata Defines the Transcriptomic Signature and Microenvironment of Early Neoplastic Lesions.Cancer discovery · 2023Article
- Epigenetic plasticity cooperates with cell-cell interactions to direct pancreatic tumorigenesis.Science (New York, N.Y.) · 2023Article
- Pancreatic cancer: Advances and challenges.Cell · 2023Review
- CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer.Cancer research · 2023Article
- Ionizable lipid nanoparticles deliver mRNA to pancreatic β cells via macrophage-mediated gene transfer.Science advances · 2023Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Pancreatic cancer is one of the most lethal malignancies, with virtually all patients eventually succumbing to their disease. Mutations in p53 have been documented in >50% of pancreatic cancers. Owing to the high incidence of p53 mutations in PanIN 3 lesions and pancreatic tumors, we interrogated the comparative ability of adult pancreatic acinar and ductal cells to respond to oncogenic Kras and mutant Tp53(R172H) using Hnf1b:CreER(T2) and Mist1:CreER(T2) mice. These studies involved co-activation of a membrane-tethered GFP lineage label, allowing for direct visualization and isolation of cells undergoing Kras and mutant p53 activation. Kras activation in Mist1(+) adult acinar cells resulted in brisk PanIN formation, whereas no evidence of pancreatic neoplasia was observed for up to 6 months following Kras activation in Hnf1beta(+) adult ductal cells. In contrast to the lack of response to oncogenic Kras alone, simultaneous activation of Kras and mutant p53 in adult ductal epithelium generated invasive PDAC in 75% of mice as early as 2.5 months after tamoxifen administration. These data demonstrate that pancreatic ductal cells, whereas exhibiting relative resistance to oncogenic Kras alone, can serve as an effective cell of origin for pancreatic ductal adenocarcinoma in the setting of gain-of-function mutations in p53.
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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.