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
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,
Introduction: The slow-growing nature of gastroenteropancreatic neuroendocrine tumours (GEP-NETs) has limited the development of clinically relevant models, hindering the discovery in the field.
Conference:
Presenting Author: Zuo X
Authors: Zuo X, Liu Y, Maxwell J, Halperin D, Dasari A,
Keywords: Well-Differentiated Gastroenteropancreatic Neuroendocrine Tumour, Patient-Derived Cancer Model, Doxycycline-Controlled Genetic Modification, Drug Screening,
Introduction: The gene mutation profiles of extra-pulmonary (EP) neuroendocrine carcinomas (NECs) and mixed neuroendocrine / non-neuroendocrine carcinomas (MiNENs) are incompletely understood.
Conference:
Presenting Author: Spada F
Authors: Spada F, Pisa E, Ranghiero A, Frassoni S, Bagnardi V,
Keywords: NEC, MiNEN, NGS, KRAS, TP53, MSI, extra-pulmonary,
#3979 New insights into the progression of NET G3 with a focus of NETs with NEC-like transformation
Introduction: Despite increasing knowledge of the clinical and morphomolecular features of NETs G3, little is known about NETs showing NEC-like transformation. Recent studies reported that NETs G3 may share histological and genetic features with NECs, such as TP53 mutations.
Conference:
Presenting Author:
Authors: Kasajima A, Moser E, Pfarr N, Ito A, Vogel L,
Keywords: Neuroendocrine Tumor, Progression, Transition, NEC-like NET,
Introduction: While gastroenteropancreatic neuroendocrine tumors (GEP-NETs) grow slowly, they are incurable when reaching advanced stages. The characteristic slow growth of GEP-NETs results in the scarcity of clinically relevant models that has hindered our comprehension of GEP-NET biology and pathology, leading to limited progress in systemic therapies of GEP-NET treatment.
Conference:
Presenting Author:
Authors: Zuo X, Liu Y, Maxwelll J, Halperin D, Dasari A,
Keywords: gastroenteropancreatic neuroendocrine tumors, patient-derived organoids, Dox-controlled genetic modifications, characterization,