Abstract library

551 results for "cell adhesion".
#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
#894 The Effects of cAMP in Different Neuroendocrine Tumorous Cells: The Role of Epac and PKA in Cell Proliferation and Cell Adhesion
Introduction: cAMP is implicated in the inhibition or stimulation of proliferation depending on cell type. Although the effects exerted by cAMP were initially attributed to the PKA activation, two cAMP-activated guanine nucleotide exchange (Epac1/2) have been later identified as cAMP targets.
Conference: 11th Annual ENETS Conference (2014)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: Eleonora Vitali
Keywords: cAMP, PKA, EPAC, GEP-NET
#801 Normal Gastrointestinal Neuroendocrine Cells Lack E-cadherin
Introduction: E-cadherin plays a crucial role in the adhesion between epithelial cells and thus epithelial integrity. Moreover, germ line mutations in the E-cadherin gene (CDH1) causing loss of E-cadherin function (adhesion) leads to hereditary gastric cancer of the diffuse type, according to Laurén. Even sporadic gastric carcinomas of the diffuse type often lose E-cadherin expression due to mutations. Lack of E-cadherin has been recorded at an early phase in such carcinomas.
Conference: 11th Annual ENETS Conference (2014)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Øyvind Hauso
#2256 Assessment of the Serum Levels of the Soluble Vascular Cellular Adhesion Molecule-1 (sVCAM-1) in Patients with Neuroendocrine Neoplasms
Introduction: Tumor growth and the ability to metastasize is a multistage process involving interactions between cancer cells and the vascular endothelium. These interactions have been reported to be mediated by various molecules including sVCAM-1. We have previously shown elevated serum concentration of sVCAM-1 in 82 neuroendocrine neoplasms (NEN) compared to controls. Here, we present results of the extension of the previous study.
Conference: 15th Annual ENETS conference (2018)
Category: Biomarkers
Presenting Author: MD PhD Violetta Rosiek
#1115 Cancer Stem Cells in Small Intestine Neuroendocrine Cell Line P-STS: Isolation and Molecular Characterisation
Introduction: Cancer stem cells (CSCs) represent a small subpopulation of tumour cells responsible for invasive tumour growth. Even though the presence of CSCs in neuroendocrine tumours is documented, their role in neuroendocrine tumourigenesis and metastasis is not defined as yet.
Conference: 12th Annual ENETS Conference (2015)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: Florian Kleinegger
#2031 Screening of Differentially Expressed Genes in Gastric Neuroendocrine Neoplasms Based on Human Transcriptome Array
Introduction: Gastric neuroendocrine neoplasms (g-NENs) are a heterogeneous group of tumors.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: Yaling Wei
Authors: Wei Y, Bai J, He N, Hua X, ...
#1528 Medullary Thyroid Carcinoma Cell Lines – An Update
Introduction: Medullary Thyroid Carcinoma (MTC) originates from calcitonin-producing neuroendocrine C-cells of the thyroid gland. Mutations in the RET-proto-oncogene are associated with both sporadic and familial MTC. As MTC are poorly responsive to chemo- and radiation- therapy, surgery is the only curative treatment at the moment. The cytogenetics of MTC have been sparsely investigated because the cells are very difficult to cultivate. In the last three decades our research group has established 10 continues cell lines derived from primary tumor and lymph node metastasis of patients with either sporadic or hereditary MTC.
Conference: 13th Annual ENETS conference (2016)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: PhD Gert Schwach
#140 Serotonin expression in gastric neuroendocrine tumors and in foci of endocrine cell hyperplasia
Introduction: The most abundant neuroendocrine (NE) cell population of the human oxyntic mucosa is the enterochromaffin-like (ECL) cells, followed by ghrelin, somatostatin and serotonin cells, respectively. All types of ECL cell carcinoids (ECL-CCs) contain serotonin cells but in a varying frequency. Hitherto, only foci of ECL and ghrelin cell hyperplasia have been described in the peritumorous mucosa of types I and II ECL-CCs. It is established that hypergastrinaemia can cause ECL cell hyperplasia but it does not affect serotonin cells. The vesicular monoamine transporter 2 (VMAT 2) is used as an immunohistochemical marker for ECL cells.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: MD, PhD Apostolos Tsolakis
Authors: Tsolakis A, Falkmer S, Grimelius L, ...
#113 Prolonged cell survival in xenografts from human digestive endocrine tumors
Introduction: Gastroenteropancreatic endocrine tumors have the capacity to achieve very large tumor masses despite usually very low proliferative rates. This suggests that neoplastic endocrine cells may have long life spans, implying the development of specific mechanisms able to promote cell survival.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Colette Roche
#1036 Abrogation of Autophagy by Chloroquine in Neuroendocrine Tumor Cells Treated with mTOR Inhibitors Induces Apoptosis, While Reduction of Cell Proliferation is Due to a Chloroquine, Autophagy Unrelated, Lysosomal Effect
Introduction: The therapy options for patients with advanced NETs are limited. The mTOR inhibitors (mTORi), Torin1 and NVP-BEZ235, are known to suppress cell proliferation in NETs. However, cancer cells may use mTORi-induced autophagy to prolong survival, evading the anti-cancer effect. Chloroquine (CQ) and hydroxychloroquine (HCQ) have been shown to inhibit autophagy.
Conference: 12th Annual ENETS Conference (2015)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: PhD Shani Avniel-Polak
Keywords: NETs, autophagy, mTORi