【摘 要】
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Background Inactivating MEN1 mutations are the most common genetic defects present in sporadic and inherited pancreatic neuroendocrine tumors (PNETs).The lack of interventional therapies prompted us t
【机 构】
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Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao-Tong
【出 处】
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中华医学会第十四次全国内分泌学学术会议
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Background Inactivating MEN1 mutations are the most common genetic defects present in sporadic and inherited pancreatic neuroendocrine tumors (PNETs).The lack of interventional therapies prompted us to explore the therapeutic approach of targeting β-catenin signaling in MEN1 mutant PNETs.Methods The phosphorylation and activation of β-catenin signaling were analyzed in human and mouse menin-deficient PNETs.Pancreatic β-cell-specific menin and β-catenin knockout and double knockout mice were used to assess the tumorigenesis, survival rate and metabolic phenotypes.Pancreas perfusion and islet transplantation in mouse models were conducted to validate the consequence of β-catenin blockage.
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