Abstract Library

#1999 Study of Cell Cycle Protein Expression Pattern in Bronchial Carcinoids: A New Potential Target for Medical Therapy?

Introduction: Bronchial Carcinoids (BCs) are rare neuroendocrine neoplasms arising from respiratory epithelium. The only effective treatment option is surgery, but its efficacy is frequently limited by metastatic spread. Everolimus prolongs progression free survival but patients may develop resistance. Previous studies demonstrated that Everolimus reduces viability of NCI-H720 cells (Atypical Carcinoid) but not of NCI-H727 cells (Typical Carcinoid). Everolimus decreases Ciclyn D1 protein levels in both cell lines but NCI-H727 cells survive, indicating a derangement in cell cycle control.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author:

Authors: Bresciani G, Riva E, Ambrosio M, Zatelli M,

Keywords: bronchial carcinoids, cell cycle, cyclins, cdks, target therapy, everolimus, dinaciclib, palbociclib,

#1637 The Effect of the Autophagy Inhibitor Chloroquine (CQ), Alone or in Combination with mTOR Inhibitors, on Neuroendocrine Tumor (NET) Growth and Metastatic Spread in Mouse Models

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,

Keywords: autophagy, mTORi, NET,

#1036 Abrogation of Autophagy by Chloroquine in Neuroendocrine Tumor Cells Treated with mTOR Inhibitors Induces Apoptosis, While Reduction of Cell Proliferation is Due to a Chloroquine, Autophagy Unrelated, Lysosomal Effect

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,

Keywords: NETs, autophagy, mTORi ,

#916 PET+10 Study: Efficacy of Platin/Etoposide Combination in Well-Differentiated Pancreatic Neuroendocrine Tumors with Ki-67 ≥ 10%

Introduction: Platin-etoposide (PE), the gold standard regimen for poorly differentiated neuroendocrine carcinomas, might be effective in well-differentiated pancreatic neuroendocrine tumors (WD-PNETs) with a high Ki-67 proliferation index.

Conference: 11th Annual ENETSConcerence (2014)

Presenting Author: BAUDIN E

Authors: Roquin G, Baudin E, Lombard-Bohas C, Cadiot G, Dominguez S,

Keywords: platin/etoposide, pNETs, Ki-67,

#815 The Effect of Autophagy Inhibitors Alone or in Combination with mTOR Inhibitors in a Neuroendocrine Tumor Cell Model

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,