Abstract Library

#4622 Elucidating the role of high mobility group box 3 (Hmgb3) during progression and response to radiation therapy in pancreatic neuroendocrine tumours

Introduction: We have recently demonstrated that HMGB3 is upregulated during the pancreatic neuroendocrine tumours (PanNETs) transition via dedifferentiation from a relatively benign molecular subtype to an aggressive and highly metastatic molecular subtype. HMGB3 expression has recently been linked to resistance to therapy, metastasis, and poor prognosis in patients with various solid cancers.

Conference:

Presenting Author: Kulathunga N

Authors: Kulathunga N, Wang Z, Qureshi A, Lok B, Tyryshkin K,

Keywords: pancreatic neuroendocrine tumour, HMGB3, tumour progression,

#4568 Investigating the dual role of SNW1 in splicing and transcription to understand pancreatic neuroendocrine tumour progression

Introduction: Pancreatic neuroendocrine tumours (PanNETs) are classified into grades (G1-G3) based on mitotic rate, with higher grades exhibiting increased dedifferentiation and invasiveness. Despite the clinical significance of PanNETs progression, the underlying mechanisms remain largely unexplored. We have previously reported that altered alternative splicing plays an essential role in PanNETs progression, where SNW1, a key regulator of splicing and transcription, was found to be overexpressed in tumour tissue, correlating with higher grade and recurrence risk.

Conference:

Presenting Author: González-Pérez C

Authors: González-Pérez C, Simón-Lesnyak M, Blázquez-Encinas R, García Vioque V, Moreno Montilla M,

Keywords: pancreas, neuroendocrine tumour, progression, SNW1, splicing,

#4158 Transcriptomic analysis of PanNET tumor progression from microtumor to metastasis in MEN1 patients

Introduction: Pancreatic Neuroendocrine Neoplasms (PanNENs) are a major component the Multiple Endocrine Neoplasia 1 Syndrome (MEN1). Although multiple pancreatic neuroendocrine microtumors (microadenomatosis) are a histomorphological hallmark of MEN1, their molecular status compared to PanNET as well as their metastasis remains unclear.

Conference:

Presenting Author:

Authors: Chouchane A, Kirchner P, Sylvain Maire R, Schiavo Lena M, Falconi M,

Keywords: Microtumor, MEN1, PanNETs, RNAseq, Transcriptomics, Progression,

#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,

#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,