Abstract library

30 results for "bon-1".
#3047 Functional Consequence of β-Arrestin 1 Gene Knock-Out in Pancreatic Neuroendocrine Tumor Cell Line BON-1
Introduction: An important limiting factor influencing treatment efficacy of neuroendocrine tumors (NETs) with somatostatin analogs (SSA) is the availability of somatostatin receptors (SSTR) on NETs. While downregulation or altered pattern of SSTR expression are important considerations, receptor internalization/desensitization by β-arrestins may be a crucial contributing factor. Interestingly, our previous study showed a preferential higher expression of β-arrestin 1 (ARRB1), in gastroenteropancreatic NETS (GEP-NETs) compared to pituitary adenomas.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Dr Anand Iyer
#775 Whole Exome Sequence Of BON-1 And QGP-1, Two Human Pancreatic Neuroendocrine Tumor Cell Lines, Reveals Homozygous Loss Of Function Mutations In TP53, HRNR and CYFIP2.
Introduction: The human BON-1 and QGP-1 cell lines are two models often used in pancreatic neuroendocrine tumor (PNET) research. Data on protein-changing mutations in these cell lines is lacking.
Conference: 10th Annual ENETS Conference 2013 (2013)
Category: Non digestive NETs (bronchial, MTC, pheochromocytoma)
Presenting Author: Timon Vandamme
#2905 DNA Methyltransferase Inhibitor Hydralazine Induces Upregulation of Somatostatin Type 2 Receptors in Human Neuroendocrine Tumor Cells
Introduction: Epidrugs like DNA methyltransferase inhibitors (DNMTi) can increase somatostatin receptor type 2 (SST2) expression in neuroendocrine tumor (NET) cells in vitro and in vivo. This effect could be used for NET patients with low SST2 expression who are currently ineligible for somatostatin analogue (SSA) treatment. However, the DNMTi known to stimulate SST2 have either a high toxicity profile or are not yet approved.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: Dr Julie Refardt
#1742 Nucleolin (NCL) Regulates Aerobic Glycolysis in Pancreatic Neuroendocrine Tumor (p-NET) BON-1 Cells
Introduction: NCL, a nucleolus localized protein and ribosomal RNA (rRNA) expression regulator, has been reported to function as an oncogene in several tumors. However, the expression and role of NCL in p-NET remains unclear.
Conference: 14th Annual ENETS conference 2017 (2017)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: Dr Kaizhou Jin
Authors: Jin K, Yu X, ...
#2988 Epigenetic Treatment with Histone Deacetylase Inhibitor Enhances Uptake of [111In]In-DOTA-TATE by Increased SST2 Expression on Neuroendocrine Tumor Cells
Introduction: The somatostatin-2 receptor (SST2) is a target for peptide receptor radionuclide therapy (PRRT) in neuroendocrine tumors (NETs). By using epigenetic drugs, which can regulate gene transcription, PRRT efficacy may be further improved due to enhanced SST2 expression.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: MSc Ilva Klomp
#466 HIF-1a Determines the Metastatic Potential of the GEP-NET Cell Line BON-1
Introduction: Intratumoral hypoxia is a hallmark of solid tumor formation and a negative predictor of patient survival. Adaptation to hypoxia is mainly achieved by the transcription factor HIF-1a, which is upregulated in a diverse range of human and experimental tumors and their metastases. HIF-1a target genes have been implicated in the induction of invasion and metastasis. However, HIF-1a’s tumor-supporting action depends on cell type and microenvironment and the precise role of HIF-1a for the pathogenesis of neuroendocrine tumors (NET) is largely unknown.
Conference: 9th Annual ENETS Conference (2012)
Category: Basic
Presenting Author: Katja Freitag de Molina
#977 Inducing, Understanding and Overcoming Resistance to Everolimus in Pancreatic Neuroendocrine Tumors
Introduction: Treatment with the mTOR-inhibitor everolimus improves progression-free survival in advanced pancreatic neuroendocrine tumors (PNETs). However, adaptive resistance to mTOR inhibition is described.
Conference: 11th Annual ENETS Conference 2014 (2014)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Timon Vandamme
Keywords: everolimus
#1737 The Role of MAPK-Signalling in Pancreatic Neuroendocrine Cancer
Introduction: Upon diagnosis, 65% of pNET patients suffer from metastatic or locally unresectable disease. The receptor tyrosine kinase inhibitor sunitinib and the mTOR inhibitor everolimus have set precedence for successful targeted therapies in pNET disease. However, response prediction and treatment alternatives still do not meet medical needs. Recent studies revealed mutations in RAS oncogenes in a fraction of tumours, emphasising a potential role of the MAPK pathway as therapeutic target.
Conference: 14th Annual ENETS conference 2017 (2017)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Julia Hoffmann
#2785 Inhibition of Cyclin Dependent Kinases Overcomes MYC-Driven Secondary Resistance to Everolimus in Digestive NETs
Introduction: Dysregulation of the mTOR pathway in digestive neuroendocrine tumours (d-NETs) led to the introduction of Everolimus (EVE) as treatment. EVE significantly increases PFS, but most patients acquire resistance, due to activation of feedback loops.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Md, PhD Gabriele Capurso
#110 Slug represents an important regulator of E-cadherin expression in neuroendocrine tumor cells of the pancreas
Introduction: Neuroendocrine tumors of the pancreas form an inhomogenous group of epithelial neoplasms. They differ from other types of pancreatic cancers by showing an extended survival of patients, which is due to a mostly slow proliferation rate of the tumor. However, some of these neuroendocrine tumors are characterized by an early onset of metastases, which cannot be predicted by any available method. The epithelial to mesenchymal transition (EMT) represents a central part of cell migration and metastasis. During EMT, cells loosen their cellular contacts, leave the tissue, and become migrating single cells. One of the integral compounds of cell adhesion represents the E-cadherin adhesion module, which contains mostly E-cadherin and several catenins. A loss of this adhesion module is associated with tumor progression, migration and metastasis in many types of cancer.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Dr Alexander König