p53 mutations cooperate with oncogenic Kras to promote adenocarcinoma from pancreatic ductal cells
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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Deletion of Trp53 in the adult ductal lineage leads to rapid development of invasive carcinoma in mice.
“the deletion of Trp53 leads to the rapid development of invasive carcinoma125–127.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [126]
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- Authors
- Bailey, J. M., Hendley, A. M., Lafaro, K. J., Pruski, M. A., Jones, N. C., Alsina, J., Younes, M., Maitra, A., McAllister, F., Iacobuzio-Donahue, C. A., & Leach, S. D.
- Affiliations
- The University of Texas Health Science Center at Houston (US)
- Memorial Sloan Kettering Cancer Center (US)
- Johns Hopkins University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Bailey, J M
- Venue
- Oncogene
- Published
- 2015-11-23
- Volume
- 35
- Issue
- 32
- Pages
- 4282-4288
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2341906519
- Cited by
- 154
- References
- 17
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 8 · 2023: 18 · 2022: 19 · 2021: 22 · 2020: 18 · 2019: 16 · 2018: 8 · 2017: 15 · 2016: 10 · 2015: 1
- FWCI
- 4.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pancreatic Cancer Action Network
- National Institutes of Health
- National Institute of General Medical Sciences (T32GM007814)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- TP53 mutation, pancreatic ductal adenocarcinoma, pancreatic intraepithelial neoplasia, pancreatic acinar cells, pancreatic ductal cells, cell of origin, tumor initiation, HNF1B, Mist1
- MeSH terms
- Adenocarcinoma, Animals, Humans, Mutation, Pancreatic Neoplasms, Phosphoproteins, Signal Transduction, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Cellular Senescence, Cell Line, Tumor, STAT3 Transcription Factor, Mice, Carcinogenesis
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