Abstract Library

Welcome to the open-access search for all ENETS abstracts presented at the Annual ENETS Conferences.

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ENETS Abstract Search

#3853 Determining the resistance to somatostatin analogues in pheochromocytomas and paragangliomas

Introduction: Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine neoplasms (NENs) derived from chromaffin cells of the neural crest. Somatostatin analogues (SSAs) represent one of the pillars for NENs diagnosis/treatment due to the high density of somatostatin receptor (SSTs) in their membrane. However, although PPGLs share this characteristic, their response to SSAs is limited, being the reason underlying this unresponsiveness still unknown.

Conference:

Presenting Author:

Authors: García Vioque V, Blázquez-Encinas R, Moreno Montilla M, Mangili F, Martínez Montes �,

Keywords: pheochromocytoma, paraganglioma, neuroendocrine tumor, somatostatin analogues, treatment resistance,

#3852 Novel insights to study the potential of the somatostatin system in NETs and NECs

Introduction: Neuroendocrine tumors (NETs) and carcinomas (NECs) are a heterogeneous group of cancers with increasing incidence worldwide. Surgery is the only curative choice, whereas an effective pharmacological approach for disseminated disease is still lacking. Somatostatin (SS) receptors (SSTs) provide a suitable pharmacological target to treat NETs with SS analogues (SSAs). However, a large proportion of NETs and, particularly most NECs, are unresponsive or resistant to SSAs. The underlying causes remain poorly understood and alternative strategies are needed. Recently, cortistatin (CST), a neuropeptide analogue of SS with comparable affinity to SSTs, emerged as an anti-inflammatory player, with potential antitumoral features.

Conference:

Presenting Author: Mangili F

Authors: Mangili F, Moreno Montilla M, García Vioque V, Blázquez-Encinas R, Mantovani G,

Keywords: PanNET, PanNEC, Somatostatin receptor (SST), cortistatin, Somatostatin,

#3505 DRD2 agonist cabergoline abolished the escape mechanism induced by mTOR inhibitor everolimus in pituitary neuroendocrine tumoral cells

Introduction: The mTOR inhibitor everolimus displays antimitotic effects on diverse neoplasms, including pituitary neuroendocrine ones (PitNETs); however, its effect is reduced by an escape mechanism that increases AKT phosphorylation (p-AKT) leading to survival pathway activation. Dopamine receptor type 2 (DRD2) reduces p-AKT in some non-functioning PitNETs (NF-PitNETs) and in lactotrophs MMQ cells, through a β-arrestin2-dependent mechanism.

Conference:

Presenting Author:

Authors: Mangili F, Esposito E, Treppiedi D, Catalano R, Marra G,

Keywords: pituitary neuroendocrine tumor, everolimus, mTOR/AKT pathway, β-arrestin 2, dopamine receptor type 2, cabergoline,