Abstract Library

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

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#4502 Molecular analysis of non-functioning PanNETs of the alpha lineage reveals new subtypes and mechanisms of progression

Introduction: Most pancreatic neuroendocrine tumours (PanNETs) are non-functioning. Previously, we demonstrated that small, MEN1-only mutated α-like PanNETs can be distinguished from larger ADM (mutated in ATRX, DAXX and MEN1) PanNETs based on epigenetic profiles. ADM PanNETs have shorter disease-free survival and a higher relapse risk. However, their therapeutic responses vary, underscoring group heterogeneity. ADM PanNETs remain insufficiently characterised, with potential subtype-specific progression drivers with implications for treatment choice and clinical outcome.

Conference:

Presenting Author: Avanthay S

Authors: Avanthay S, Di Domenico A, Kirchner P, Bräutigam K, Chouchane A,

Keywords: pancreas, epigenetics, progression, metastasis, DAXX, ATRX, Pan NET,

#3388 Epigenetic progression steps in alpha-lineage MEN1-DAXX/ATRX mutated Pancreatic Neuroendocrine Tumors (PanNET)

Introduction: Recently, based on DNA methylation profiles, we have hypothesized that PanNETs with mutations in ATRX, DAXX and MEN1 originate from α-cells. Alpha-like PanNETs, small and indolent, were enriched for mutations in MEN1 only, while epigenetically intermediate PanNETs, larger and with high relapse risk, showed mutations in both MEN1 and DAXX/ATRX (Int-ADM). Int-ADM PanNETs show progressive loss of alpha cell differentiation.

Conference:

Presenting Author: Marinoni I

Authors: Di Domenico A, Kirchner P, Maire R, Thirlwell C, Perren A,

Keywords: Epigenetics, DAXX/ATRX, PanNET, PanNET progression,

#2906 Change of Lactate Transporter (MCT4) Expression in Pancreatic Microadenomas and Stages of Pancreatic Neuroendocrine Tumors

Introduction: Metabolic changes are observed in early and late stages of Pancreatic Neuroendocrine Tumors (PanNET) in mouse models. In human PanNET, RNA-expression analysis showed changes in glucose metabolism in more aggressive PanNET.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Bräutigam K

Authors: Straub J, Bräutigam K, Di Domenico A, Galván J, Maire R,

Keywords: metabolism, microadenoma, immunohistochemistry, pancreas, tumor, mct4, relapse,

#2739 Epigenetic Landscape of Pancreatic Neuro-Endocrine Tumors Reveals Distinct Cells of Origin and Means of Tumor Progression

Introduction: Pancreatic Neuroendocrine Tumors (PanNETs) arise from cells of the Islets of Langerhans. The majority of PanNETs are non-functional and their cell of origin cannot be defined analysing specific hormone production. Cell of origin assessment has proven importance to identify risk factors, prevent tumour development, and tailor treatment in many malignancies. Recent data on super-enhancer signatures has suggested a potential origin of PanNET from α- or β-cells. We and others have shown that distinct epigenetic profiles assessed by DNA methylation (DNAme) characterize genomic and prognostic groups of PanNET.

Conference: 17th Annual ENETSConcerence (2020)

Presenting Author: Di Domenico A

Authors: Di Domenico A, Pipinikas C, Maire R, Bräutigam K, Vassella E,

Keywords: cell of origin, alpha, beta, methylation, expression, epigenetic, neuroendocrine, progression, PanNET, tumor,

#2128 Epigenetic Changes in DAXX and/or ATRX Negative Pancreatic Neuro-Endocrine Tumors

Introduction: The most commonly mutated genes in Pancreatic Neuroendocrine Tumors (PanNETs) are MEN1, DAXX and ATRX, which encode for proteins involved in epigenetic regulation. DAXX/ATRX mutated PanNETs are globally hypomethylated and behave clinically in a more aggressive way. Tumor pathways associated with these changes are still unclear. We hypothesize that DAXX/ATRX and MEN1 mutations mediate PanNET progression via epigenetic dysregulation.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Di Domenico A

Authors: Di Domenico A, Pipinikas C, Simillion C, Wiedmer T, Maire R,

Keywords: methylation, expression, miRNA, epigenetic, PanNETs, neuroendocrine, tumors, MEN1, DAXX, ATRX, progression,