The DOI matches its Crossref record; 39 of the 40 references it cites were found in a registry or an index.
Pancreatitis-Induced Inflammation Contributes to Pancreatic Cancer by Inhibiting Oncogene-Induced Senescence
Open accessAbstract
Pancreatic acinar cells of adult mice (≥P60) are resistant to transformation by some of the most robust oncogenic insults including expression of K-Ras oncogenes and loss of p16Ink4a/p19Arf or Trp53 tumor suppressors. Yet, these acinar cells yield pancreatic intraepithelial neoplasias (mPanIN) and ductal adenocarcinomas (mPDAC) if exposed to limited bouts of non-acute pancreatitis, providing they harbor K-Ras oncogenes. Pancreatitis contributes to tumor progression by abrogating the senescence barrier characteristic of low-grade mPanINs. Attenuation of pancreatitis-induced inflammation also accelerates tissue repair and thwarts mPanIN expansion. Patients with chronic pancreatitis display senescent PanINs, providing they have received antiinflammatory drugs. These results support the concept that antiinflammatory treatment of people diagnosed with pancreatitis may reduce their risk of developing PDAC.
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In the citing paper
“Tumor development in adult mice, however, can be greatly accelerated by chemically induced pancreatitis.”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [81]
In the citing paper
“Thus, inflammatory signaling is likely to play a critical role in pancreatic cancer development (80, 81).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [81]
In the citing paper
“pancreatic acinar cells, in which Kras-G12V is activated during adulthood, exhibit a low frequency of PanIN development and resistance to transformation, at least in part due to OIS 118”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [118]
In the citing paper
“episodic pancreatitis induced by caerulein, a decapeptide analog of the gastrointestinal peptide hormone cholecystokinin, inhibited the OIS program, thus facilitating malignant transformation in this model 118”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [118]
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Metadata
- Authors
- Guerra, C., Collado, M., Navas, C., Schuhmacher, A. J., Hernández-Porras, I., Cañamero, M., Rodriguez-Justo, M., Serrano, M., & Barbacid, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Corresponding author
- Guerra, Carmen
- Barbacid, Mariano
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 19
- Issue
- 6
- Pages
- 728-739
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC4890723
- OpenAlex
- W1965887568
- Cited by
- 516
- References
- 40
- Citations by year
- 2026: 17 · 2025: 20 · 2024: 31 · 2023: 40 · 2022: 22 · 2021: 44 · 2020: 36 · 2019: 41 · 2018: 27 · 2017: 36 · 2016: 22 · 2015: 37 · 2014: 65 · 2013: 38 · 2012: 33
- FWCI
- 22.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 813 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- European Research Council (ERC-AG/250297-RAS AHEAD)
- Ministerio de Ciencia e Innovación (CSD2007-00017, SAF2006-11773)
- INCLIVA Instituto de Investigación Sanitaria (ERC-AG/233270, GR/SAL/0349/2004, PI042124, SAF2008-02959)
- Fundación Mutua Madrileña
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- pancreatitis, pancreatic cancer, oncogene-induced senescence, inflammation, pancreatic intraepithelial neoplasia, K-ras oncogene, chronic pancreatitis, anti-inflammatory agents, tissue repair, tumor progression, p16INK4a, Trp53, pancreatic ductal adenocarcinoma
- MeSH terms
- Adenocarcinoma, Animals, Anti-Inflammatory Agents, Cell Transformation, Neoplastic, Humans, Pancreatic Neoplasms, Pancreatitis, Genes, ras, Genes, p53, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Carcinoma, Pancreatic Ductal, Pancreas, Exocrine, Mice
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