Critical focus on mechanisms of resistance and toxicity of m-TOR inhibitors in pancreatic neuroendocrine tumors

Pancreatic neuroendocrine tumors (pNETs) are rare neoplasms arising from pancreatic endocrine cells and accounting for less than 2% of all pancreatic malignancies [1]. The phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is often deregulated in pNETs and seems to play a key role in the tumorigenesis [2,3]. In a phase III, randomized, double-blind, placebo-controlled study (RADIANT-3) the mTOR inhibitor everolimus in combination with best supportive care (BSC) demonstrated a significantly prolonged progression-free survival (PFS) compared to placebo and BSC in patients affected by locally advanced or metastatic, radiologically progressing, well/moderately differentiated pNETs.

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