Abstract Library
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Introduction: mTOR inhibitors (mTORi) such as RAD001 demonstrated promising anti-cancer effect in NETs. Autophagy, a cell survival mechanism, is activated by mTORi. We have recently shown in the human NET cell line BON1 that autophagy is essential for cell survival. Treatment with CQ alone or together with mTORi robustly inhibited cell proliferation and survival, suggesting that treatment with CQ may potentiate the anti-tumorigenic effects of mTORi.
Conference: 14th Annual ENETSConcerence (2017)
Presenting Author: Avniel-Polak S
Authors: Avniel-Polak S, Leibowitz G, Gross D, Grozinsky-Glasberg S,
Introduction: The therapy options for patients with advanced NETs are limited. The mTOR inhibitors (mTORi), Torin1 and NVP-BEZ235, are known to suppress cell proliferation in NETs. However, cancer cells may use mTORi-induced autophagy to prolong survival, evading the anti-cancer effect. Chloroquine (CQ) and hydroxychloroquine (HCQ) have been shown to inhibit autophagy.
Conference: 12th Annual ENETSConcerence (2015)
Presenting Author: Avniel- Polak S
Authors: Avniel-Polak S, Leibowitz G, Glaser B, Gross D, Grozinsky-Glasberg S,
Introduction: Most patients with neuroendocrine tumors (NETs) require systemic treatment, often with a limited therapeutic effect. RAD001 and Torin1 are mTOR inhibitors (mTORi) known to suppress cell proliferation in NETs. However, cancer cells may use mTORi-induced autophagy to escape the anti-proliferative effect and to prolong cell survival. Chloroquine (CQ) and hydroxychloroquine (HCQ) inhibit autophagy.
Conference: 11th Annual ENETSConcerence (2014)
Presenting Author: Glasberg S
Authors: Avniel-Polak S, Leibowitz G, Glaser B, Gross D, Glasberg S,
Keywords: NETs, autophagy, mTOR inhibitors,