Abstract Library

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

Everyone can browse the library to find basic information on abstracts. To get full access to each entry, you will be asked to log in to your myENETS account.

 

Please note:

Participants of the 2025 ENETS Conference enjoy full access to the 2025 conference digital resources through myENETS: the abstract booklet, e-posters and videos, slide decks of talks, the poster carousel, and more.

ENETS Abstract Search

#4545 Analysis of the mutational landscape of pancreatic neuroendocrine tumours before and after temozolomide treatment

Introduction: Temozolomide (TMZ) is an alkylating agent and standard treatment for pancreatic neuroendocrine tumours (pNET). Resistance to TMZ may be acquired through inactivation of the mismatch repair system, leading to high tumour mutation burden (hTMB).

Conference:

Presenting Author: Trevisani E

Authors: Trevisani E, Borghesani M, Reni A, Agnoletto C, Luchini C,

Keywords: neuroendocrine, next generation sequencing, temozolomide, hypermutation, tumour mutational burden,

#4289 Temozolomide-associated hypermutation and response to immunotherapy in advanced pulmonary neuroendocrine tumours

Introduction: Temozolomide (TMZ) cytotoxicity depends on an intact DNA mismatch repair (MMR) pathway and low levels of O6-methylguanine DNA methyltransferase (MGMT). However, absence of MGMT-mediated repair coupled with defective MMR (dMMR) may lead to enrichment of C:G to A:T transitions throughout the genome, a marked increase in tumour mutational burden (TMB), and loss of TMZ-induced cytotoxicity. This resistance mechanism is called TMZ-associated hypermutation (TAH). Theoretically, this effect could lead to sensitivity to checkpoint inhibitor immunotherapy.

Conference:

Presenting Author: Buikhuisen W

Authors: Buikhuisen W, Badrising S, Moonen L, Derks J, Monkhorst K,

Keywords: Pulmonary NET, whole genome sequencing, temozolomide signature, immunotherapy,

#4194 Temozolomide treatment induces an MMR-dependent hypermutator phenotype in well-differentiated pancreatic neuroendocrine tumors

Introduction: Temozolomide (TMZ), an alkylating agent, is an effective treatment used in multiple tumor types including advanced pancreatic neuroendocrine tumors (PanNET). In glioblastomas, TMZ induces a hypermutator and hyperprogressor phenotype in a subset of patients through MMR deficiency. In advanced colon cancer, TMZ priming increases tumor mutational burden (TMB), favouring immunotherapy efficacy.

Conference:

Presenting Author: de Mestier L

Authors: de Mestier L, Cohen D, de Rycke O, Masliah Planchon J, Fleischmann Z,

Keywords: temozolomide, hypermutation, pancreatic neuroendocrine tumor,