Abstract Library
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ENETS Abstract Search
Introduction: Altered expression of Insulin-like Growth Factor-1 (IGF-1), its receptor (IGF-1R), Connective Tissue Growth Factor (CTGF) and Hypoxia Factor-1 (HIF-1), has been implicated in tumorigenesis. These factors have not been studied systematically in Pulmonary Carcinoids (PCs).
Conference: 15th Annual ENETSConcerence (2018)
Presenting Author:
Authors: Tsolakis A, Kanakis G, Grimelius G, Papaioannou D, Kaltsas G,
Introduction: Several studies have shown altered expression of Insulin-like Growth Factor-1 (IGF-1) and its receptor (IGF-1R) in different types of cancers. Connective Tissue Growth Factor (CTGF) is triggered by Serotonin (5-HT) and Hypoxia Induced Factor 1 (HIF-1) and has been associated with tumor expansion and desmoplastic reaction in carcinoid tumors.
Conference: 11th Annual ENETSConcerence (2014)
Presenting Author:
Authors: Kanakis G, Grimelius L, Kaltsas G, Tsolakis A,
#233 Afinitor UK Particular Patient Supplies for Advanced Neuroendocrine Tumors (NETs)
Introduction: The PI3/Akt/mTOR pathway is activated by IGF-1 in NETs. mTOR regulates signalling downstream of IGF-1R1: Afinitor and Sandostatin may synergistically arrest growth and secretory activity in NETs.
Conference: 8th Annual ENETSConcerence (2011)
Presenting Author:
Authors: Chambers J,
Keywords: Afinitor, neuroendocrine tumors ,
Introduction: Insulin-like growth factor-1 receptor (IGF-1R) was reported to be expressed in NET (neuroendocrine tumor) cells but its biological roles and activation status in non-functioning NET are unknown.
Conference: 8th Annual ENETSConcerence (2011)
Presenting Author:
Authors: Sasano H, Iida S, Ono K, Nakamura Y, Miki Y,
Keywords: IGF-1R, mTOR, non-functioning neuroendocrine tumor, immunohistochemistry,
Introduction: Targeting of multiple pathways has become an important strategy for improved tumor control in metastatic neuroendocrine tumors (NETs). Among these targets is the mammalian target of rapamycin (mTOR), a central regulator of cell growth, proliferation, and apoptosis, which is blocked by everolimus, an oral inhibitor of mTOR that has shown efficacy in patients with metastatic pancreatic NETs. Recent evidence has suggested that suppression of insulin-like growth factor-1 receptor (IGF-1R) secretion with octreotide therapy, along with concurrent inhibition of mTOR by everolimus, may improve tumor control synergistically by preventing feedback activation of the PI3K/Akt/mTOR pathway.
Conference: 7th Annual ENETSConcerence (2010)
Presenting Author:
Authors: Teulé Vega A, Ochoa M, Villabona C, Cuadra C, Salazar Soler R,
Keywords: pancreatic neuroendocrine tumor, everolimus, octreotide LAR, case study,