Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with limited therapeutic options. However, metabolic adaptation to the harsh PDAC environment can expose liabilities useful for therapy. Targeting the key metabolic regulator mechanistic target of rapamycin complex 1 (mTORC1) and its downstream pathway shows efficacy only in subsets of patients but gene modifiers maximising response remain to be identified.
Lysosomal lipid switch sensitises to nutrient deprivation and mTOR targeting in pancreatic cancer / De Santis, Maria Chiara; Gozzelino, Luca; Margaria, Jean Piero; Costamagna, Andrea; Ratto, Edoardo; Gulluni, Federico; Di Gregorio, Enza; Mina, Erica; Lorito, Nicla; Bacci, Marina; Lattanzio, Rossano; Sala, Gianluca; Cappello, Paola; Novelli, Francesco; Giovannetti, Elisa; Vicentini, Caterina; Andreani, Silvia; Delfino, Pietro; Corbo, Vincenzo; Scarpa, Aldo; Porporato, Paolo Ettore; Morandi, Andrea; Hirsch, Emilio; Martini, Miriam. - In: GUT. - ISSN 0017-5749. - ELETTRONICO. - (2022), pp. 0-0. [10.1136/gutjnl-2021-325117]
Lysosomal lipid switch sensitises to nutrient deprivation and mTOR targeting in pancreatic cancer
Lorito, Nicla;Bacci, Marina;Porporato, Paolo Ettore;Morandi, Andrea;Martini, Miriam
2022
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with limited therapeutic options. However, metabolic adaptation to the harsh PDAC environment can expose liabilities useful for therapy. Targeting the key metabolic regulator mechanistic target of rapamycin complex 1 (mTORC1) and its downstream pathway shows efficacy only in subsets of patients but gene modifiers maximising response remain to be identified.
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