Abstract Library

#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,

#1462 Cross-Talk Between EGFR and IGF1R Influences the Response to RTK Inhibitors in Bronchopulmonary (BP)-NET Cell Lines

Introduction: BP-NETs represent ~30% of all neuroendocrine tumors. BP-NET treatment is challenging due to onset of resistance to chemo and targeted therapies. EGFR and IGF1R had been associated with tumor onset and progression in several neoplasia.

Conference: 13th Annual ENETSConcerence (2016)

Presenting Author: Gagliano T

Authors: Gagliano T, Gentilin E, Benfini K, Falletta S, Di Pasquale C,

Keywords: BP-NET RTK,

#1301 Role of TSC22D1 (TGFβ-Stimulated Clone 22 Domain Family Member 1) in Bronchial Carcinoids

Introduction: Neuroendocrine tumors (NETs) include bronchial carcinoids, either typical (TC) or atypical (AC). Tsc22d1 encodes for a member of TSC22 domain family of leucine zipper transcription factors; the protein (TSC22D1) is stimulated by TGFβ. Microarray data analysis obtained comparing a pool of TC tissue specimens with a pool of AC tissue specimens shows TSC22D1 down-regulation in AC samples. These data were confirmed by real time PCR and Western blot in vitro models of TC (NCI-H727 cells) and AC (NCI-H720 cells)

Conference: 13th Annual ENETSConcerence (2016)

Presenting Author:

Authors: Falletta S, Gagliano T, Di Pasquale C, Benfini K, Riva E,

Keywords: TSC22D1, bronchial carcinoid, TGFβ,

#1173 Investigation of the Effects of Sunitinib on Pheochromocytoma and Paraganglioma Primary Cultures

Introduction: The main treatment for Pheochromocytoma and Paraganglioma is surgery. However these tumors are highly vascularized, suggesting the possible role for anti-angiogenic agents in the medical therapy. Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor (TKI), mainly described to inhibit VEGFR

Conference: 12th Annual ENETSConcerence (2015)

Presenting Author:

Authors: Bellio M, Gagliano T, Feo C, Balboni F, Gentilin E,

Keywords: Sunitinib, Pheochromocytoma, Paraganglioma ,