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oai:repisalud.isciii.es:20.500.12105/230722024-11-29T13:50:46Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc 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 author 2011-06-14 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. 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 Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.