作者: Li Ding , Lingling Han , Yin Li , Jing Zhao , Ping He
DOI: 10.1016/J.NEO.2014.08.010
关键词: Metastasis 、 Cancer research 、 PI3K/AKT/mTOR pathway 、 Neoplasm 、 TSC1 、 Progenitor cell 、 Genetically modified mouse 、 Pancreas 、 Sirolimus 、 Biology
摘要: The role of tuberous sclerosis complex (TSC) in the pathogenesis pancreatic cancers remains largely unknown. present study shows that neurogenin 3 directed Cre deletion Tsc1 gene induces development acinar carcinoma. By cross-breeding Neurog3-cre mice with Tsc1loxp/loxp mice, we generated Neurog3-Tsc1−/− transgenic which is deleted and mTOR signaling activated progenitor cells. All developed notable adenocarcinoma-like lesions pancreas starting from age 100 days old. tumor are composed cells morphological molecular resemblance to Metastasis neoplasm liver lung was detected 5% animals. Inhibition by rapamycin significantly attenuated growth neoplasm. Relapse occurred within 14 days upon cessation treatment. Our studies indicate activation may trigger Thus, serve as a potential target for treatment