Abstract Library

#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,

#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,

#2988 Epigenetic Treatment with Histone Deacetylase Inhibitor Enhances Uptake of [111In]In-DOTA-TATE by Increased SST2 Expression on Neuroendocrine Tumor Cells

Introduction: The somatostatin-2 receptor (SST2) is a target for peptide receptor radionuclide therapy (PRRT) in neuroendocrine tumors (NETs). By using epigenetic drugs, which can regulate gene transcription, PRRT efficacy may be further improved due to enhanced SST2 expression.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Klomp I

Authors: Klomp I, Dalm S, van Koetsveld P, Dogan-Oruç F, de Jong M,

Keywords: neuroendocrine tumors, bon-1, epigenetic, histone, histone deacetylase inhibitor, HDACi, upregulation, reversibility, somatostatin receptor-2, somatostatin,

#2908 Re-Cellularised Human Pancreas 3D Scaffolds as a Novel Model for Biomarker Discovery in Pancreatic Neuroendocrine Tumours (pNETs)

Introduction: The lack of preclinical models of pNETs has challenged identification of tissue specific biomarkers of disease. Culturing cancer cells in their native tissue enables the close study of cell-ECM interaction and tissue remodelling. The biological products of such interactions can form a basis for discovery of novel biomarkers of the disease, and were previously linked with a range of inflammatory and malignant conditions.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Ney A

Authors: Ney A, Al-Akkad W, Frenguelli L, Acedo P, Mazza G,

Keywords: 3d models, pancreatic neuroendocrine tumors, Biomarkers,

#2905 DNA Methyltransferase Inhibitor Hydralazine Induces Upregulation of Somatostatin Type 2 Receptors in Human Neuroendocrine Tumor Cells

Introduction: Epidrugs like DNA methyltransferase inhibitors (DNMTi) can increase somatostatin receptor type 2 (SST2) expression in neuroendocrine tumor (NET) cells in vitro and in vivo. This effect could be used for NET patients with low SST2 expression who are currently ineligible for somatostatin analogue (SSA) treatment. However, the DNMTi known to stimulate SST2 have either a high toxicity profile or are not yet approved.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Refardt J

Authors: Refardt J, Klomp I, van Koetsveld P, Dogan-Oruç F, de Herder W,

Keywords: somatostatin type 2 receptor, BON-1, GOT-1, upregulation, DNA methyltransferase inhibitor, histone deacetylase inhibitor, epigenetic,