Abstract Library

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

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ENETS Abstract Search

#4524 SIRT7 drives the radioresistance of pancreatic neuroendocrine tumours via the DNMT1-MEN1 axis

Introduction: Pancreatic neuroendocrine tumours (PanNETs) are a rare and highly heterogeneous type of tumour in the pancreas. After failure of standard treatment, patients have poor prognoses. Radiotherapy may be a potential therapeutic modality for such patients. However, PanNETs usually exhibit a radiation “cold” tumour through unclarified mechanisms.

Conference:

Presenting Author: Jianyun J

Authors: Jiang J, Xu J, Liang Y, Chen L, Ji S,

Keywords: pancreatic neuroendocrine tumour, radio resistance, SIRT7, MEN1,

#4355 Emergence of DNA damage repair clonal haematopoiesis after peptide receptor radionuclide therapy for neuroendocrine tumours

Introduction: In neuroendocrine tumours (NETs), PRRT (Peptide Receptor Radionuclide Therapy), has shown efficacy but with significant hematologic toxicity. Clonal haematopoiesis (CHIP) is considered a risk factor for therapy-related myeloid neoplasms (t-MN).

Conference:

Presenting Author: Hadoux J

Authors: Loyaux R, Hadoux J, Oziel-Taieb S, Durand A, Bouhier Leporrier K,

Keywords: PRRT, clonal haematopoiesis, DNA Damage Repair, therapy-related myeloid neoplasm, Neuroendocrine tumour,

#4189 Pit and pitfalls of tumor mutational burden assessment in well-differentiated pancreatic neuroendocrine tumors: Two case reports from University of Verona

Introduction: The hypermutated phenotype is used as a predictive parameter for immune-checkpoint inhibitors (ICI). However, the relationship between high TMB, the underlying mutational drivers and response to ICI is still unclear.

Conference:

Presenting Author: Trevisani E

Authors: Torresan I, Reni A, Trevisani E, Borghesani M, Rossi A,

Keywords: Neuroendocrine tumor, NGS, Tumor Mutational Burden, Alkylating agent, DNA Damage Repair, Liquid biopsy,

#4182 DNA damage repair genes alterations in pancreatic neuroendocrine tumor treated with Temozolomide

Introduction: Temozolomide (TMZ), a standard therapy for pancreatic neuroendocrine tumors (pNETs), is an alkylating agent causing missense mutations and triggering cell death.

Conference:

Presenting Author: Trevisani E

Authors: Trevisani E, Reni A, Torresan I, Borghesani M, Rossi A,

Keywords: DNA Damage Repair, Tumor mutational burden, Neuroendocrine, Temozolomide,

#2280 The BON-SSTR2 Chicken Chorioallantoic Membrane (CAM) Model for the Analysis of Lu-17-DOTATOC Sensitizing Agents

Introduction: Peptide radioreceptor therapy (PRRT) is a promising therapy option for SSTR2-positive pancreatic neuroendocrine neoplasms (NEN). However, therapeutic effects are often not satisfying concerning sensitivity to PRRT. We hypothesize that the slow proliferation of NENs provides sufficient time for the repair of beta-particle induced-DNA damage. The ubiquitin-proteasome-system is involved in DNA damage repair and affected by the proteasome inhibitor bortezomib (Velcade®). The inhibition of DNA damage repair during PRRT may be an option to improve therapy response in NEN. We have recently demonstrated the damage repair inhibitory and pro-apoptotic effect of bortezomib in NEN in vitro (Briest et al., in revision).

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Briest F

Authors: Briest F, Grötzinger C, Exner S, Sedding D, Baum R,

Keywords: peptide radioreceptor therapy, Lu-177-DOTATOC, PRRT, bortezomib, in vivo model, SPECT/CT Imaging, chicken CAM model, Sensitizer, DNA damage repair,