Abstract Library

#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,

#2279 Expression of FOXM1 in G3 Neuroendocrine Tumors (NET G3) and G3 Neuroendocrine Carcinomas (NEC G3) of the Pancreas and the Intestine

Introduction: G3 gastroenteropancreatic neuroendocrine tumors (G3 NET) and carcinomas (G3 NEC) differ considerably concerning their biological behavior and patients outcome. Whereas the WHO2017 classification for pancreatic NETs proposes a distinction of both groups using the Ki-67 proliferation marker (Klöppel et al. Reviews and Reports 2017), a useful marker for the subclassification of G3 intestinal NETs have not been recommended until now.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Briest F

Authors: Briest F, Konukiewitz B, Anlauf M, Klöppel G, Grabowski P,

Keywords: gastroenteropancreatic neuroendocrine tumors, GEP-NET, NET G3, NEC G3, Tumor marker, FOXM1, Ki-67, differentiation,

#2275 Analysis of Gene Expression Patterns of Rectum Neuroendocrine Tumors (NET) Versus Healthy Tissue Reveals Alterations in the MAPK and WNT Signaling Pathways

Introduction: The neuroendocrine tumors (NETs) of the rectum are rare but increasing in incidence, by means of improved endoscopic techniques and histological reporting. They often occur as small polypoid lesions and G1, and in most cases an incidental finding at endoscopy.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Briest F

Authors: Briest F, Hummel M, Grabowski P, Arsenic R,

Keywords: rectum neuroendocrine tumors, NET, MAP kinase, gene expression analysis, Wnt signaling,

#1542 Selective Inhibition of PI3Kalpha (BYL719) - Promising Therapeutic Option for Neuroendocrine Tumors?

Introduction: Neuroendocrine tumors are heterogeneous, often functional malignancies and their therapeutic options are limited. As the PI3 kinase signaling is ­in GEP-NENs, selective PI3Kalpha inhibitors may be more potent than panPI3K inhibitors.

Conference: 13th Annual ENETSConcerence (2016)

Presenting Author: Grabowski P

Authors: Nölting S, Rentsch J, Freitag H, Briest F, Schrader J,

Keywords: PI3Kalpha, BYL719, neuroendocrine tumor cell lines,

#1507 The CDK4/6 Inhibitor Palbociclib Induces Anti-proliferative Mechanisms in Gastroenteropancreatic Neuroendocrine Neoplasms In Vitro

Introduction: Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are rare tumors with heterogeneous molecular backgrounds and mostly unknown druggable driver mutations. Especially for the midgut NENs effective treatment options are limited. The retinoblastoma pathway is often inactive due to CDK4/6 overexpression in pancreatic NENs. Palbociclib is a FDA approved (ER-positive and HER2-negative breast cancer) cyclin-dependent kinases 4 and 6 inhibitor and might impair cell cycle progression and proliferation.

Conference: 13th Annual ENETSConcerence (2016)

Presenting Author: Briest F

Authors: Briest F, Grass I, Siegmund B, Grabowski P,

Keywords: GEP-NEN, targeted therapy, cyclin-dependent kinases 4/6,