Abstract
Introduction: Pancreatic adenocarcinoma shows high resistance to traditional apoptosis inducing chemotherapeutic agents due to activation of multiple proliferative pathways downstream of K-ras, including PI3K/AKT/mTOR as well as high expression of BCl-2. Recently mTOR inhibition has shown promise in the treatment of pancreatic neuroendocrine tumors, but trials of mTOR complex 1 (mTORC1) inhibitors in the treatment of pancreatic ductal adenocarcinoma have not demonstrated efficacy. We hypothesized that newer classes of dual mTOR inhibitors may be more effective in suppressing PDAC growth and that the combination of the mTOR inhibitors with the anti-autophagy compound chloroquine (ChQ) would enhance cell death induced by mTOR inhibition.
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