期刊
CANCER CELL
卷 22, 期 3, 页码 318-330出版社
CELL PRESS
DOI: 10.1016/j.ccr.2012.08.001
关键词
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资金
- European Research Council [ERC-AG/250297-RAS AHEAD]
- EU [LSHG-CT-2007-037665, HEALTH-F2-2010-259770, HEALTH-2010-260791]
- Spanish Ministry of Science and Innovation [SAF2006-11773, CSD2007-00017]
- Spanish Ministry of Economy and Competitiveness [SAF2011-30173]
- 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, PI08-1623]
- Fundacion Ramon Areces [FRA 01-09-001]
- Doctoral Program Inflammation and Immunity [DK W1212]
- EC program [LSHC-CT-2006-037731]
- Austrian Federal Government's GEN-AU program Austro-mouse [GZ 200.147/1-VI/1a/2006, 820966]
Clinical evidence indicates that mutation/activation of EGF receptors (EGFRs) is mutually exclusive with the presence of K-RAS oncogenes in lung and colon tumors. We have validated these observations using genetically engineered mouse models. However, development of pancreatic ductal adenocarcinomas driven by K-Ras oncogenes are totally dependent on EGFR signaling. Similar results were obtained using human pancreatic tumor cell lines. EGFRs were also essential even in the context of pancreatic injury and absence of p16Ink4a/p19Arf. Only loss of p53 made pancreatic tumors independent of EGFR signaling. Additional inhibition of PI3K and STAT3 effectively prevented proliferation of explants derived from these p53-defective pancreatic tumors. These findings may provide the bases for more rational approaches to treat pancreatic tumors in the clinic.
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