Abstract Library

#4381 TOPK promotes tumorigenesis and metastasis of pancreatic neuroendocrine neoplasms by enhancing the MAPK signalling pathway

Introduction: T-LAK cell-originated protein kinase (TOPK) is highly expressed in pancreatic neuroendocrine neoplasms (pNENs) with liver metastasis and is associated with a poor prognosis.

Conference:

Presenting Author: Chen Q

Authors: Chen Q, Yuan M, Meng M, Ren S, Li G,

Keywords: TOPK, Pancreatic Neuroendocrine Neoplasm, MAPK signalling pathway, Invasion and metastasis, HI-TOPK-032,

#3997 FOXA2-initiated transcriptional activation of INHBA induced by methylmalonic acid promotes pancreatic neuroendocrine neoplasm progression

Introduction: More than 60% of pancreatic neuroendocrine neoplasms (PanNENs) represent metastases when diagnosed. Metabolic alterations have been recognized as one of the hallmarks of tumor metastasis. However, little is known about the molecular mechanism of metabolic changes regulating PanNEN progression.

Conference:

Presenting Author:

Authors: Hu C,

Keywords: metabolic alteration, tumor progression, pancreatic neuroendocrine neoplasm, FOXA2, INHBA, epithelial-mesenchymal transition,

#3934 The stromal microenvironment endows pancreatic neuroendocrine tumors with spatially specific invasive and metastatic phenotypes

Introduction: Cancer-associated fibroblasts (CAFs) play an important role in a variety of cancers. However, the heterogeneity of CAFs is poorly understood in non-functional pancreatic neuroendocrine tumors (NF-PanNETs). Profiling the heterogeneity of CAFs might reveal the causes of malignant phenotypes in NF-PanNETs.

Conference:

Presenting Author: Ye Z

Authors: Ye Z, Zhou C, Xu X, Chen J, Yu X,

Keywords: nonfunctional pancreatic neuroendocrine tumors, TGF-β, epithelial-mesenchymal transition,

#3713 Methylmalonic acid activates INHBA induced epithelial-mesenchymal transition and promotes the cancer progression by TGF-β signalling pathway in pancreatic neuroendocrine neoplasm

Introduction: Metabolic reprogramming is a well-recognized hallmark of cancer progression, especially the process of tumor metastasis. However, the role of metabolic alteration and its potential mechanism in pancreatic neuroendocrine neoplasm (pNEN) with metastasis remain elusive.

Conference:

Presenting Author: Hu C

Authors: Hu C, Ye M, Bai J, Tang Q,

Keywords: metabolic reprogramming, pancreatic neuroendocrine neoplasm, methylmalonic acid, INHBA, TGF-β, epithelial-mesenchymal transition,

#1847 CXCR4 Inhibition by Ulocuplumab Prevents EMT of pNET Cells in Vitro

Introduction: Neuroendocrine tumors (NETs) overexpress CXCR4. We have previously shown that stimulation of CXCR4 by its ligand SDF-1 promotes the epithelial-mesenchymal transition (EMT) and increases distant tumor spread. Ulocuplumab (Ulo) is a fully human IgG4 mAb designed to inhibit the binding of CXCR4 to SDF-1.

Conference: 14th Annual ENETSConcerence (2017)

Presenting Author: Quaresmini D

Authors: Quaresmini D, Cives M, Pellè E, Ungaro A, Felici C,

Keywords: pNET, CXCR4, EMT, Ulocuplumab,