期刊
CANCER CELL
卷 19, 期 6, 页码 728-739出版社
CELL PRESS
DOI: 10.1016/j.ccr.2011.05.011
关键词
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资金
- EU [LSHG-CT-2007-037665]
- European Research Council [ERC-AG/250297-RAS AHEAD, ERC-AG/233270]
- Spanish Ministry of Science and Innovation (MICINN) [SAF2006-11773, CSD2007-00017]
- Autonomous Community of Madrid [GR/SAL/0587/2004, S2006/BIO-0232, GR/SAL/0349/2004]
- Fundacion de la Mutua Madrilena del Automovil
- Fondo de Investigacion Sanitaria [PI042124]
- MICINN [CSD2007-00017, SAF2008-02959]
- Marcelino Botin Foundation
- UCLH/UCL Comprehensive Biomedical Research Centre (London, UK)
- MCINN
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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