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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“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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Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses
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Hingorani, S. R., Petricoin, E. F., Maitra, A., Rajapakse, V., King, C., Jacobetz, M. A., Ross, S., Conrads, T. P., Veenstra, T. D., Hitt, B. A., et al. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00309-x · Cited by 2,471
Pancreatitis and the Risk of Pancreatic Cancer
Lowenfels, A. B., Maisonneuve, P., Cavallini, G., Ammann, R., Lankisch, P. G., Andersen, J. R., DiMagno, E. P., Andrén‐Sandberg, Å., & Domellöf, L. (1993) · New England Journal of Medicine · doi:10.1056/nejm199305203282001 · Cited by 1,753
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Senescence in premalignant tumours
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Self-citationGuerra, C., Schuhmacher, A. J., Cañamero, M., Grippo, P. J., Verdaguer, L., Pérez-Gallego, L., Dubus, P., Sandgren, E. P., & Barbacid, M. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.01.012 · Cited by 1,224
Self-citationSenescence in tumours: evidence from mice and humans
Collado, M., & Serrano, M. (2010) · Nature Reviews Cancer · doi:10.1038/nrc2772 · Cited by 1,124 · cited 4×
“The Senescence Program Present in Low-Grade mPanIN Is Abrogated during Progression to High-Grade mPanIN Lesions Metaplasias and low-grade mPanINs observed in mice expressing K-RasG12V since embryonic development display senescence markers similar to those present in preneoplastic stages of other tumor types (Collado a…”
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Accessories to the Crime: Functions of Cells Recruited to the Tumor Microenvironment
Hanahan, D., & Coussens, L. M. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.02.022 · Cited by 4,632
Özdemir, B. C., Pentcheva-Hoang, T., Carstens, J. L., Zheng, X., Wu, C.-C., Simpson, T. R., Laklai, H., Sugimoto, H., Kahlert, C., Novitskiy, S. V., et al. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.04.005 · Cited by 2,681
EMT and Dissemination Precede Pancreatic Tumor Formation
Rhim, A. D., Mirek, E. T., Aiello, N. M., Maitra, A., Bailey, J. M., McAllister, F., Reichert, M., Beatty, G. L., Rustgi, A. K., Vonderheide, R. H., et al. (2012) · Cell · doi:10.1016/j.cell.2011.11.025 · Cited by 2,136
Cellular senescence and the senescent secretory phenotype: therapeutic opportunities
Tchkonia, T., Zhu, Y., van Deursen, J., Campisi, J., & Kirkland, J. L. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64098 · Cited by 1,774
Signaling in innate immunity and inflammation
Newton, K., & Dixit, V. M. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a006049 · Cited by 1,513
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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