Abstract Library

Members may log into MY ENETS to visit the abstract library from previous ENETS conferences.

Participants of the ENETS Conference in 2022 can now access the abstract booklet, e-posters and videos, the poster carousel, and more via My ENETS.

ENETS Abstract Search

#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,

#2126 Histone Replacement in Cancer: Dissecting the Role of H3.3 Chaperones in Pancreatic Tumorigenesis

Introduction: Cancer driver mutations affecting the histone H3.3 chromatin remodellers ATRX and DAXX were recently discovered in 43% of sporadic pancreatic neuroendocrine tumours (PNET). Progressive age-dependent replacement of canonical H3.1/2 with H3.3 is crucial for maintaining genome integrity through expression of repressive markers at heterochromatic sites, where loading is mediated by ATRX and DAXX. Loss of H3.3 chaperones in PNET is associated with activation of ALT, a telomere maintenance mechanism, eventually leading to chromosome instability. It has been suggested that ATRX/DAXX expression is necessary for repressing ALT, but mechanistic details of this interaction are not fully understood.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Sposito T

Authors: Sposito T, C Nguyen Tu M, Thirlwell C, Salomoni P,

Keywords: PNET, mouse model, epigenetic,

#1587 LRIG1 Was Down-Regulated in Medullary Thyroid Cancer but No Significant Effect of LRIG1 Was Found in RET2B Transgenic Mice and Human Differentiated Thyroid Cancer

Introduction: There are four main types of thyroid cancer, papillary (PTC), follicular (FTC), medullary (MTC), and anaplastic. In both PTC and MTC, genomic rearrangements and point mutations in the proto-oncogene RET are common. RET encodes a receptor tyrosine kinase that is negatively regulated by leucine-rich repeats and immunoglobulin-like domains-1 (LRIG1). LRIG1 gene status and mRNA and protein expression correlate with patient survival in different types of cancer.

Conference: 14th Annual ENETSConcerence (2017)

Presenting Author: Lindquist D

Authors: Lindquist D, Henriksson R, Hedman H,

Keywords: LRIG1, RET, MTC,

#387 Combined Blockade of Several Signalling Pathways Shows Marked Anti-Tumor Potential in Two Novel Mouse Phaeochromocytoma Cell Lines

Introduction: The current study explores novel targeted therapies for malignant pheochromocytomas (PCCs) and paragangliomas, utilizing a more benign (MPC) and a more malignant (MTT) PCC cell line. We have previously shown that the dual PI3K/mTORC1 inhibitor NVP-BEZ235 significantly reduced MPC and MTT cell viability, but increased ERK signalling.

Conference: 9th Annual ENETSConcerence (2012)

Presenting Author:

Authors: Noelting S, Garcia E, Alusi G, Korbonits M, Grossman A,

Keywords: pheochromocytoma, cell lines, proliferation, MAPK, mTOR,

Abstract Submissions in 2023

Abstract submissions for 2023 will open in September 2022!

 

The 20th Annual ENETS Conference in 2023 will provide the principal platform for NET researchers around the world to present their latest findings. ENETS will select the best abstracts submitted in both clinical and basic science and present these in sessions within the framework of its scientific programme.

 

Participants of the ENETS Conferences in 2022 can now access the abstract booklet, e-posters and videos, the poster carousel, and more via My ENETS.

Membership matters

Multidisciplinary is our credo. We welcome all NET-related disciplines and professionals! Learn more about the benefits of becoming an ENETS member.