Cholangiocarcinoma (CCA) is still a deadly tumour. Histological and molecular aspects of thioacetamide (TAA)-induced intrahepatic CCA (iCCA) in rats mimic those of human iCCA. Carcinogenic changes and therapeutic vulnerabilities in CCA may be captured by molecular investigations in bile, where we performed bile proteomic and metabolomic analyses that help discovery yet unknown pathways relevant to human iCCA.
New molecular mechanisms in cholangiocarcinoma: signals triggering interleukin-6 production in tumor cells and KRAS co-opted epigenetic mediators driving metabolic reprogramming / Colyn, Leticia; Alvarez-Sola, Gloria; Latasa, M Ujue; Uriarte, Iker; Herranz, Jose M; Arechederra, Maria; Vlachogiannis, George; Rae, Colin; Pineda-Lucena, Antonio; Casadei-Gardini, Andrea; Pedica, Federica; Aldrighetti, Luca; López-López, Angeles; López-Gonzálvez, Angeles; Barbas, Coral; Ciordia, Sergio; Van Liempd, Sebastiaan M; Falcón-Pérez, Juan M; Urman, Jesus; Sangro, Bruno; Vicent, Silve; Iraburu, Maria J; Prosper, Felipe; Nelson, Leonard J; Banales, Jesus M; Martinez-Chantar, Maria Luz; Marin, Jose J G; Braconi, Chiara; Trautwein, Christian; Corrales, Fernando J; Cubero, F Javier; Berasain, Carmen; Fernandez-Barrena, Maite G; Avila, Matias A. - In: JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH. - ISSN 1756-9966. - 41:1(2022). [10.1186/s13046-022-02386-2]
New molecular mechanisms in cholangiocarcinoma: signals triggering interleukin-6 production in tumor cells and KRAS co-opted epigenetic mediators driving metabolic reprogramming
Casadei-Gardini, Andrea;Pedica, Federica;Aldrighetti, Luca;
2022-01-01
Abstract
Cholangiocarcinoma (CCA) is still a deadly tumour. Histological and molecular aspects of thioacetamide (TAA)-induced intrahepatic CCA (iCCA) in rats mimic those of human iCCA. Carcinogenic changes and therapeutic vulnerabilities in CCA may be captured by molecular investigations in bile, where we performed bile proteomic and metabolomic analyses that help discovery yet unknown pathways relevant to human iCCA.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
