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.

 

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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

#4654 Usefulness of soluble tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) and its receptors R2 and R3 in progression assessment of gastroenteropancreatic neuroendocrine neoplasms – A preliminary study

Introduction: TRAIL is a member of TNF family and appears in membrane and soluble (s) forms. It acts either triggering (R1 and R2) or blocking (R3 and R4) apoptosis. TRAIL targeted therapy is widely studied and known as potentially effective in number of neoplasms.

Conference:

Presenting Author: Kaczmarska-Turek D

Authors: Kaczmarska-Turek D, Radziszewski M, Matałowski M, Liszcz A, Bartoszewicz Z,

Keywords: gastroenteropancreatic neuroendocrine neoplasm, tumour necrosis factor-related apoptosis-inducing ligand, tumour progression, PRRT, TRAIL, GEP-NEN,

#4436 Application of novel wound materials in symptom management of patients with neuroendocrine tumours

Introduction: Neuroendocrine tumours can occur in multiple parts of the body, and management faces challenges.

Conference:

Presenting Author:

Authors: Liu G, Gu T, Tang Y, Xie W, Zhu Y,

Keywords: neuroendocrine tumour, novel wound materials, symptom management,

#4373 Focal adhesion kinase drives proliferation and invasion in gastrointestinal neuroendocrine tumours via modulation of transformative cell signalling and gene expression

Introduction: Focal Adhesion Kinase (FAK) is a non-receptor protein kinase that localises in both the cytoplasm and nucleus, influencing cell function through its enzymatic and scaffold activities. Through its scaffold function, FAK modulates gene expression epigenetically. Gastrointestinal neuroendocrine tumours (GI-NETs) exhibit a relatively low mutation rate, supporting the hypothesis that these malignancies may be driven epigenetically. Recently, PROTAC (PROteolysis TArgeting Chimeras) technology has enabled selective inhibition and degradation of FAK, providing a novel approach to explore its role in GI-NETs.

Conference:

Presenting Author: Gagliano T

Authors: Toffoli L, Ditsiou A, Moschioni E, Hamm V, Gagliano T,

Keywords: FAK, GI-NET, Cell Signalling, Epigenetics,

#3966 PTK2 PROTAC unveiled as a selective inhibitor of gastrointestinal neuroendocrine cell proliferation via multi-target drug screening

Introduction: Gastrointestinal neuroendocrine tumors (GI-NETs) exhibit a complex and diverse nature, posing challenges in their effective treatment and management. While there have been advancements in treatment options, addressing the need for more effective and targeted therapies remains a significant issue, especially for patients with advanced or metastatic disease. Improving outcomes in the management of patients with GI-NETs is a key priority, and further research and development are crucial in this regard.

Conference:

Presenting Author: Gagliano T

Authors: Malavasi E, Toffoli L, Dainotto M, Gagliano T,

Keywords: Protac, PTK2, Screening, GI-NETs,

#3724 Tackling drug activity and resistance mechanisms in neuroendocrine tumors treated with cabozantinib

Introduction: Neuroendocrine tumors (NETs) are highly vascularized malignancies and angiogenesis plays a relevant role in cell proliferation and survival. Nowadays, innovative therapies have amplified the paradigm treatment of NETs. Among the compounds with anti-vascular properties, cabozantinib (CAB) appeared promising.

Conference:

Presenting Author: Cella C

Authors: Cella C, Cazzoli R, Fazio N, de Petro G, Gaudenzi G,

Keywords: Neuroendocrine tumor, angiogenesis, zebrafish model, mouse model.,