Abstract library

39 results for "copy-number alterations".
#2234 High Rate of Copy-Number Alterations in Gastrointestinal and Pancreatic Neuroendocrine Tumors with Unidentified Driver Mutations
Introduction: The driving genetic alteration leading to neuroendocrine tumor (NET) development has been reported for primary tumors of pancreatic origin, but not for metastases. Moreover, even for primary tumor a significant “dark matter” remains to be explored.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: Dr Amit Tirosh
Authors:
#2196 The Neuroendocrine Phenotype, Genomic Profile, and Therapeutic Sensitivity of GEPNET Cell Lines
Introduction: Patient tumour-derived cell lines have been widely used for studying the molecular mechanisms of tumours and their response to therapy. The establishment of cell lines from gastro-entero-pancreatic neuroendocrine tumours (GEPNETs) has proved difficult, but despite the challenges a limited amount of cell lines now exists.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: Tobias Hofving
Authors:
#471 Alterations of Global and Gene-Specific DNA Methylation in Midgut Carcinoids
Introduction: Epigenetic alterations of DNA methylation are known to be associated with the clinical presentation of midgut carcinoids.
Conference: 9th Annual ENETS Conference (2012)
Category: Basic
Presenting Author: Omid Fotouhi
Authors:
#87 Alterations of E-cadherin, beta-catenin and caveolin-1 expression in gastroenteropancreatic neuroendocrine tumors
Introduction: Gastroenteropancreatic neuroendocrine tumors (GEP NETs) comprise a heterogeneous group of neoplasm with different histological patterns and biological behavior. Only limited information is available on immunohistochemical prognostic factors of disease. Alterations in the cell-cell adhesion system are closely associated with cell invasion and metastasis in many malignancies, including those of endocrine origin. Abnormal expression of E-cadherin and beta-catenin has been reported to play an important role in these processes. Caveolin-1 has recently been identified as a tumor metastasis modifier factor, which might increase the cell metastasis potential through the interaction with E-cadherin. However, the role of caveolin-1 in GEP NETs cell invasion remains unknown.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Vera V Delektorskaya
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#1490 Even Malignant Appendiceal Neuroendocrine Tumors Exhibit No Recurrent Chromosomal Alterations
Introduction: Neuroendocrine tumors (NETs) of the midgut are located in the ileum (iNET), caecum or appendix (aNET). Despite of the similar origin, NETs of the ileum and the appendix behave remarkably different. iNETs show high malignant potential, which manifests with early lymph node or liver metastases. Genetically, the loss of chromosome 18 (Ch18) in 60-74% of cases is the most frequent alteration in iNETs. aNETs are often incidental findings, rarely show metastases, and no chromosomal alterations are known.
Conference: 13th Annual ENETS conference (2016)
Category: Basic Science - Genetics, epigenetics, miRNAs
Presenting Author: Maike Nieser
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Keywords: NET
#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 ENETS conference (2018)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Dr. Franziska Briest
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#264 Alterations of TIMP-3 Gene in Insulinomas and Its Significance
Introduction: Our previous study on insulinoma found allelic loss of 22q12 where suppressor gene TIMP3 located. TIMP3 can inhibit tumor invasion or metastasis, but its clinical implications in insulinoma are unknown.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Dr Yuan-Jia Chen
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#564 Genetic Alterations in Glucagon Cell Adenomatosis
Introduction: Glucagon cell adenomatosis (GCA) was recently recognized by us as a multifocal neoplastic disease of the endocrine pancreas unrelated to MEN-1. Multiple micro- and a few macrotumors are found on the background of a hyperplasia of glucagon cells. The disease may cause unspecific abdominal symptoms and only rarely a glucagonoma syndrome. Recently a mutation in the glucagon receptor (GCGR) gene was described in one GCA
patient.
Conference: 9th Annual ENETS Conference (2012)
Category: Clinical
Presenting Author: Dr. Tobias Henopp
Authors:
Keywords: glucagon
#1843 Infrastructural Alterations in Insulinoma
Introduction: Insulinomas are the most frequent functioning pancreatic endocrine tumors
Conference: 14th Annual ENETS conference (2017)
Category: Pathology, grading, staging
Presenting Author: Oxana Paklina
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#65 Deletions of 11q21-q25 are associated with atypical lung carcinoids and a poor clinical outcome
Introduction: Lung carcinoids comprise a group of smoking-unrelated neuroendocrine tumors, which can be classified in typical (TC) and atypical (AC) carcinoids. Classification is complex and its accuracy to predict disease outcome is variable. In a previous array comparative genomic hybridization (arrayCGH) study, we showed that the average number of chromosomal alterations (≥ 1Mb) was significantly higher in ACs than in TCs (512 v. 226 per tumor) and that the most common region of chromosome loss was 11q21-q25 (Neuroendocrinology 2009;90:136-137).
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: MSc Dorian RA Swarts
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