Abstract Library

#3067 Somatostatin Analogs in Real‐World Practice for Patients with Metastatic Neuroendocrine Tumors: A Single Institution Experience in the Ouest of Algeria (CHU Oran)

Introduction: The efficacy of somatostatin analogs (SSAs) were clearly established trough pivotal trials as first‐line agents for neuroendocrine tumors (NETs), but their use in clinical practice is largely unknown.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author:

Authors: Ameziane N, Behourah Z, Aida M, Ahed Messaoud M, Bousahba A,

Keywords: GEP-NET, Somatostatin analogs, anti proliferative action, anti secretory action, Management real world practice,

#3062 The Splicing Factor CELF4 Is Dysregulated in Neuroendocrine Tumors, Where It Can Enhance Aggressiveness Features

Introduction: There is increasing evidence that alterations in alternative splicing are linked to key tumor features in different cancers. Besides mutations, dysregulation of the splicing machinery would represent the main underlying cause for these alterations. Indeed, splicing dysregulation is emerging as a novel, transversal cancer hallmark, due to its association with multiple dysfunctions in tumor cells.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Alors-Pérez E

Authors: Alors-Pérez E, Pedraza-Arévalo S, Vázquez-Borrego M, Blázquez-Encinas R, Herrera-Martínez A,

Keywords: PanNET, CELF4, splicing, aggressiveness, pituitary tumors,

#3056 Multi-Omic Characterization and Evolution of Neuroendocrine Neoplasm Organoids

Introduction: Molecular characterizations of neuroendocrine neoplasm (NENs) have unveiled candidate alterations associated with aggressiveness and suggested that the molecular link between neuroendocrine tumors (NETs) and neuroendocrine carcinomas (NECs) might be subtler than initially thought. For example, we have recently unveiled a new entity of pulmonary carcinoids (supra-carcinoids) with carcinoid-like morphology yet the molecular and clinical features of large cell neuroendocrine carcinoma (LCNEC). Testing hypotheses to explain aggressiveness and the possibility of progression or transition from NET to NEC through the accumulation of genetic anomalies requires in vitro and in vivo experimental models.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Foll M

Authors: Alcala N, Dayton T, Mangiante L, Delhomme T, Tabone-Egling S,

Keywords: organoids, omics, evolution, lung, pancreas, bioinformatics,

#3053 The Splicing Machinery Is Dysregulated in Low Grade Pulmonary Neuroendocrine Tumors

Introduction: Alternative splicing dysregulation is increasingly regarded as a novel cancer hallmark influencing all key tumor features. We have shown that neuroendocrine tumors (NETs) overexpress aberrantly spliced variants of neuropeptides and receptors that increase tumor malignancy. More recently, we discovered that the splicing machinery is dysregulated in pituitary and pancreatic NETs. To date, the status of this machinery in low grade pulmonary NETs is largely unknown.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Blázquez-Encinas R

Authors: Blázquez-Encinas R, Caro M, Pedraza-Arévalo S, Alors-Pérez E, Herrera-Martínez A,

Keywords: low grade pulmonary NETs, splicing, splicing machinery, malignancy,

#3047 Functional Consequence of β-Arrestin 1 Gene Knock-Out in Pancreatic Neuroendocrine Tumor Cell Line BON-1

Introduction: An important limiting factor influencing treatment efficacy of neuroendocrine tumors (NETs) with somatostatin analogs (SSA) is the availability of somatostatin receptors (SSTR) on NETs. While downregulation or altered pattern of SSTR expression are important considerations, receptor internalization/desensitization by β-arrestins may be a crucial contributing factor. Interestingly, our previous study showed a preferential higher expression of β-arrestin 1 (ARRB1), in gastroenteropancreatic NETS (GEP-NETs) compared to pituitary adenomas.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Iyer A

Authors: Iyer A, Vriens J, Dogan-Oruç F, van Koetsveld P, Hofland L,

Keywords: β-arrestin 1, CRISPR-Cas9, BON-1, knock-out, SSTR, SSA, Pan-NET,