Abstract Library

#2980 Metabolic Dysregulation and Circadian Clock in Cellular Models of Neuroendocrine Tumors

Introduction: The circadian clock genes encode transcription factors whose interaction with nuclear receptors allows the regulation of cellular metabolism.The invalidation of the genes of the clock core is associated with the development of many endocrine diseases including neuroendocrine cancer. Recently, the family of transcriptional coactivators PGC-1a has been identified as a key element in the integration of cellular metabolic state with the circadian clock. PRC, as a member of the PGC-1 family, was able to interact with several transcription factors, including the CLOCK factor. The specific induction of this PRC factor by the cell cycle, to modulate the energy function, the MAPkinase pathway and the expression of microRNAs, makes it a key factor in the metabolic adaptation of cancer cells.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Savagner F

Authors: Savagner F, Le Pennec S,

Keywords: Metabolism, Circadian clock, cell models,

#2785 Inhibition of Cyclin Dependent Kinases Overcomes MYC-Driven Secondary Resistance to Everolimus in Digestive NETs

Introduction: Dysregulation of the mTOR pathway in digestive neuroendocrine tumours (d-NETs) led to the introduction of Everolimus (EVE) as treatment. EVE significantly increases PFS, but most patients acquire resistance, due to activation of feedback loops.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Capurso G

Authors: Terracciano F, Capone A, Montori A, Pilozzi E, Arcidiacono P,

Keywords: mTOR, Myc, resistance, pathway, RNA-seq,

#2291 Somatostatin Analogs and mTOR Inhibitors as Radioprotectors or Radiosensitizers in Neuroendocrine Tumor Cells

Introduction: Neuroendocrine tumors (NETs) express somatostatin receptors that are currently utilized for diagnostic and therapeutic approaches. For peptide receptor radionuclide therapy (PRRT), somatostatin analogs are coupled to radionuclides like 90Y or 177Lu, which after injection are bound and taken up specifically by NETs. One hypothesis potentially explaining the discrepancies between expected result and observed outcome of PRRT might be that somatostatin analogs induce a G1 arrest in NET cells, thereby rendering them radioresistant.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Grötzinger C

Authors: Grötzinger C, Exner S, Prasad V, Erdmann S, Wiedenmann B,

Keywords: PRRT,

#2233 Potential Effects of Ketoconazole on ACTH-Producing and Non-ACTH-Producing Neuroendocrine Tumors

Introduction: Prolonged biochemical remission after treatment with steroidogenesis inhibitors has been described in patients with Cushing’s syndrome due to ectopic adrenocorticotropin hormone (ACTH) production. Some studies have suggested antiproliferative and apoptotic effect of ketoconazole in human cancer cells.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Herrera-Martínez A

Authors: Herrera-Martínez A, Feelders R, Castaño J, Van Dungen R, Dogan-Oruc F,

Keywords: ACTH- and non-ACTH producing NETs, ketoconazole, somatostatin analogs, apoptosis, cytotoxicity,

#2101 The Effect of Temozolomide on Pancreatic Neuroendocrine Tumors in Vitro and Role of MGMT and MMR System in Temozolomide Resistance

Introduction: Temozolomide (TMZ) has been suggested as a treatment option for patients with pancreatic neuroendocrine tumours (PNETs). The tumour response to TMZ has been linked to expression levels of O6-methylguanine-DNA methyltransferase (MGMT) and components of the mismatch repair (MMR) system.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Blazevic A

Authors: Blazevic A, Dogan-Oruc F, Dedeci M, Van Koetsveld P, Feelders R,

Keywords: Pancreatic neuroendocrine tumors, Temozolomide, Cell lines, Tumor growth, O6-methylguanine-DNA methyltransferase (MGMT), Mismatch repair (MMR) system,