Abstract Library

#3320 TGF-β increase caspase activation and migration in typical bronchial carcinoids

Introduction: Typical bronchial carcinoids (TBC) are well-differentiated neuroendocrine neoplasms (NEN) whose management can still be very challenging due to reduced sensitivity to therapy. Previous studies have reported TGF-β’s ability to activate mTOR pathway and induce epithelial to mesenchymal transition (EMT). Moreover, preliminary results show an overexpression of TGF-β signalling and caspase activation in TBC.

Conference: 18th Annual ENETS Concerence (2021)

Presenting Author: Gagliardi I

Authors: Borges de Souza P, Gagliardi I, Martelli M, Zatelli M,

Keywords: bronchial carcinoid, TGF-β signalling, mTOR, EMT,

#3065 Intensive Personalized Program for Daily Living with Neuroendocrine Neoplasms as a Chronic Disease: Preliminary Results

Introduction: Introduction: Neuroendocrine neoplasms (NENs) are increasingly viewed as chronic diseases as a result of more effective treatments and procedures. As with any life changing events, patient and family transition to a new “normal” requires attitudinal adjustments. The Intensive Personalized Program for Daily Living with Neuroendocrine Neoplasms is a pilot program transitioning patients and their primary familial carer to a new “normal”.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Rosenberg M

Authors: Rosenberg M, Whyand T, Grozinsky-Glasberg S,

Keywords: QoL, Quality of Life, NEN Dietitian, PRO, Patient Reported Outcomes,

#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,

#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,