Are eIFs Ingredients for Neuroendocrine Tumorigenesis? Abstract #1320

Introduction: Neuroendocrine tumors (NETs) develop in almost any organ, therefore they are a very heterogeneous group of tumors. One of the major activities in every cell is the translation of mRNA to the corresponding protein, which plays an important role in cancer development. Crucial for this translation process are eukaryotic initiation factors (eIFs), which are themselves regulated by the mammalian target of Rapamycin (mTOR)-pathway. Mutation or deregulated expression of eIFs influences cell growth and proliferation, contributing to carcinogenesis. The incidence of NETs has increased fivefold over the last three decades.
Aim(s): We aimed at investigating the contribution of eIFs to NETs.
Materials and methods: NETs and their metastases from 3 individuals were analyzed on protein expression level for eIFs and mTOR members by Western Blot. Additionally we have investigated various eIF subunits in gastroenteropancreatic NETs and neuroendocrine carcinomas by immunohistochemistry. Normal adjacent tissue served as control.
Conference: 13th Annual ENETS conference (2016)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: MSc. Nadine Gantenbein

To read results and conclusion, please login ...

Further abstracts you may be interested in

#726 Expression and Phosphorilation of mTOR Pathway and Antitumor Activity of mTOR Inhibitors in Neuroendocrine Tumors
Introduction: The mammalian target of rapamycin (mTOR) is a protein kinase involved in the control of cancer cell metabolism, growth and proliferation. The mTOR pathway has attracted broad scientific and clinical interest, particularly in light of the ongoing clinical cancer trials with mTOR inhibitors in pts with neuroendocrine tumors (NETs). To identify the best candidates for treatment with mTOR inhibitors is challenging.
Conference: 10th Annual ENETS Conference (2013)
Category: Epidemiology/Natural history/Prognosis - Registries, nationwide and regional surveys
Presenting Author: Concetta Sciammarella
#1109 Expression and Role of the CXCR4/CXCL12/CXCR7 Axis and Crosstalk with the mTOR Pathway in Neuroendocrine Tumors (NETs)
Introduction: Chemokine receptor CXCR4 has been shown to signal on mTOR pathway in gastric and renal cancer. CXCR4 interacts with the chemokine CXCL12 to exert proliferative and chemotactic effects.
Conference: 12th Annual ENETS Conference (2015)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: student Concetta Sciammarella
#860 Expression and Prognostic Role of CXCR4/CXCL12/CXCR7 and mTOR Pathways in Neuroendocrine Tumors (NETs)
Introduction: The chemokine receptor CXCR4 interacts with the ligand CXCL12 to exert proliferative and chemotactic effects. CXCR4 activates mTOR through phosphorylation of its two effectors downstream:4EBP1and S6K
Conference: 11th Annual ENETS Conference (2014)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Doctor Luisa Circelli
#220 The Global mTOR Inhibitor Torin1 is More Effective than the mTORC1 Inhibitor, Everolimus, Alone or in Combination with Histone Deacetylases Inhibitors, in Suppressing Neuroendocrine Tumors Cell Proliferation
Introduction: Torin1, a new mTOR inhibitor that globally inhibits both mTORC1 and mTORC2, seems to impair cell growth and proliferation to a greater degree than rapamycin; its effects in NET cells are unknown.
Conference: 8th Annual ENETS Conference (2011)
Category: Basic
Presenting Author: Dr. Simona Grozinsky-Glasberg
#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