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Abstract Hyperactivation of the mechanistic target of rapamycin (mTOR) complexes, mTORC1 and mTORC2, is common in pancreatic ductal adenocarcinoma (PDAC). However, clinical use of mTOR inhibitors has shown limited efficacy due to rapid adaptive resistance. Using inducible genetically engineered mouse models and matched organoids, we delineated distinct complex-specific adaptations.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
