2026-05-17T00:18:30Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/230722024-11-29T13:50:46Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Guerra, Carmen
author
Collado, Manuel
author
Navas, Carolina
author
Schuhmacher, Alberto J
author
Hernández-Porras, Isabel
author
Cañamero, Marta
author
Rodriguez-Justo, Manuel
author
Serrano, Manuel
author
Barbacid, Mariano
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Comunidad de Madrid (España)
funder
Ministerio de Ciencia y Competitividad (España)
funder
Marcelino Botin Foundation
funder
UCLH/UCL Comprehensive Biomedical Research Centre (London, UK)
2024-09-16T08:16:54Z
2024-09-16T08:16:54Z
2011-06-14
Cancer Cell . 2011;19(6):728-39
10.1016/j.ccr.2011.05.011
1878-3686
Cancer cell
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890723/pdf/emss-52291.pdf
21665147
https://hdl.handle.net/20.500.12105/23072
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.
eng
Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.
research article