Abstract Library

#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,

#1638 3D Primary Cell Culture: A New Promising Preclinical Model for Pancreatic Neuro-Endocrine Tumors (pNETs).

Introduction: The lack of adequate in vitro and in vivo preclinical models has hampered the identification of novel treatment options and the development of personalized therapy selection for pNET patients.

Conference: 14th Annual ENETSConcerence (2017)

Presenting Author:

Authors: Marinoni I, Mooser C, Wiedmer T, Di Domenico A, Pantasis S,

Keywords: pNET, preclinical models, 3D culture.,

#1312 Epigenetic Remodeling upon DAXX and ATRX Loss in Pancreatic Neuro-endocrine tumors (pNETs)

Introduction: DAXX and or ATRX loss occur in 40% of sporadic pNETs. DAXX and ATRX participate in the cell epigenetic status maintenance. Epigenetic changes influence gene expression, function of telomeres and genomic stability. We hypothesize that DAXX/ATRX loss drives tumor progression in pNET through epigenetic changes affecting genomic stability.

Conference: 13th Annual ENETSConcerence (2016)

Presenting Author:

Authors: Marinoni I, Wiederkeher A, Pantasis S, Normand L, Wiedmer T,

Keywords: DAXX/ATRX, epigenetic, CIN,

#1111 Autophagy as a Possible Mechanism of Resistance in pNET Treatment

Introduction: Pancreatic neuroendocrine tumor (pNET) patients often display primary or secondary resistance to Sunitinib, an anti-angiogenic multi-receptor tyrosine kinase inhibitor which has been approved for the treatment of late stage pNETs. In late cancer stage autophagy often has a tumor promoting role. Sunitinib might additionally activate autophagy through inhibition of mTOR or induction of hypoxia.

Conference: 12th Annual ENETSConcerence (2015)

Presenting Author:

Authors: Wiedmer T, Marinoni I, Tschan M, Perren A,

Keywords: pNET, autophagy, Sunitinib, resistance,