KRAS is mutated in the majority of pancreatic ductal adenocarcinoma. MAPK and PI3K-AKT are primary KRAS effector pathways, but combined MAPK and PI3K inhibition has not been demonstrated to be clinically effective to date. We explore the resistance mechanisms uniquely employed by malignant cells.

Identification of Resistance Pathways Specific to Malignancy Using Organoid Models of Pancreatic Cancer

Corbo, Vincenzo;Filippini, Dea;
2019-01-01

Abstract

KRAS is mutated in the majority of pancreatic ductal adenocarcinoma. MAPK and PI3K-AKT are primary KRAS effector pathways, but combined MAPK and PI3K inhibition has not been demonstrated to be clinically effective to date. We explore the resistance mechanisms uniquely employed by malignant cells.
2019
MOUSE MODEL; PI3K INHIBITION; MEK INHIBITION; RAS ONCOGENES; KRAS; COMBINATION; GROWTH; CHEMOTHERAPY; GEMCITABINE; ARRY-142886
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/1010303
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