Abstract library

8 results for "autophagy".
#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 ENETS Conference (2014)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Dr. Simona Glasberg
#1559 MTOR Controls an Epigenetic Program Leading to Autophagy and Cell Growth Control
Introduction: Makroautophagy represents an evolutionary highly conserved process involved in the clearance of proteins and organelles. The induction of this central cellular process is tightly connected with programs regulating cell growth control. While the cytoplasmic machinery that orchestrates autophagy is relatively well understood the key epigenetic events that initiate autophagy-related cell growth programs remain largely unknown.
Conference: 13th Annual ENETS conference (2016)
Category: Basic Science - Genetics, epigenetics, miRNAs
Presenting Author: Dr. Alexander Koenig
#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 ENETS Conference (2015)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: PhD Shani Avniel-Polak
Keywords: NETs, autophagy, mTORi
#1111 Autophagy as a Possible Mechanism of Resistance in pNET Treatment
Introduction: Pancreatic neuroendocrine tumor (pNET) patients often display primary or secondary resistance to Sunitinib, an anti-angiogenic multi-receptor tyrosine kinase inhibitor which has been approved for the treatment of late stage pNETs. In late cancer stage autophagy often has a tumor promoting role. Sunitinib might additionally activate autophagy through inhibition of mTOR or induction of hypoxia.
Conference: 12th Annual ENETS Conference (2015)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Tabea Wiedmer
#2030 Autophagy Process in Pancreatic Neuroendocrine Tumor Cells
Introduction: Pancreatic neuroendocrine malignancy is rising up in the last decade. Despite surgical resection and palliative therapy, an effective therapy has not been developed yet.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: PhD Pietro Di Fazio
#2073 Epigenetic Modulation of Autophagy in Pancreatic Spheroid Cells
Introduction: Pancreatic neuroendocrine malignancy is rising up in the last decade. Despite surgical resection and palliative therapy, an effective therapy has not been developed yet.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: PhD Pietro Di Fazio
#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 ENETS conference (2017)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: MD Simona Grozinsky-Glasberg
Keywords: autophagy, mTORi, NET
#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 ENETS conference (2018)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Giulia Bresciani
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