2026-08-29T15:34:07Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/230712024-11-29T15:03:08Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Navas, Carolina
author
Hernández-Porras, Isabel
author
Schuhmacher, Alberto J
author
Sibilia, Maria
author
Guerra, Carmen
author
Barbacid, Mariano
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Ministerio de Economía y Competitividad (España)
funder
Instituto de Salud Carlos III
funder
Fundacion de la Mutua Madrilena del Automovil
funder
Fundacion Ramon Areces
funder
Austrian Federal Government's GEN-AU program "Austro-mouse"
2024-09-16T08:16:54Z
2024-09-16T08:16:54Z
2012-09-11
Cancer Cell . 2012 ;22(3):318-30
10.1016/j.ccr.2012.08.001
1878-3686
Cancer cell
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601542/pdf/emss-52254.pdf
22975375
https://hdl.handle.net/20.500.12105/23071
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.
eng
EGF receptor signaling is essential for k-ras oncogene-driven pancreatic ductal adenocarcinoma.
research article