Abstract library

1928 results for "Pancreatic neuroendocrine tumors".
#11 Plasma chromogranin - A response to octreotide test: Prognostic value for clinical outcome in endocrine digestive tumors
Introduction: Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) expressing somatostatin receptors may be treated with somatostatin analogues (SSAs). Selection criteria are a positive Octreoscan® or a >50% hormone level decrease after octreotide s.c. injection (octreotide test) (OT). Plasma chromogranin A (CgA) is the best general GEP-NET marker, but data on CgA response to OT are scant.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD, PhD Sara Massironi
#16 Endoglin as indicator of metastatic neuroendocrine tumors of the pancreas
Introduction: Neuroendocrine tumors of the pancreas are rare, highly vascularized tumors. Endoglin, a Transforming Growth Factor-β co-receptor, is a marker for angiogenic endothelial cells. Angiogenesis is required for tumor progression and the development of metastases. Recently, endoglin expression was found to be a prognostic marker in pancreatic carcinomas. However, the role of endoglin in neuroendocrine pancreatic tumors has so far not been studied.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Patricia Kuiper
#61 Multiple tumors in patients with pancreatic neuroendocrine tumours: morphological and immunohistochemical characteristics
Introduction: Pancreatic islet cell tumors occur in 80% of patients with MEN 1. Tumors are often multicentric. They often produce multiple peptides and biogenic amines.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Prof Larisa Gurevich
#62 Genome-wide DNA methylation profiling of pancreatic neuroendocrine tumors identifies distinct methylation profiles and differentially methylated gene promoter regions associated with low, medium and high grade tumors
Introduction: Integration of genetics and epigenetics has emerged as a powerful approach to studying cellular differentiation (Mikkelsen et al, 2009) and tumorigenesis (Shen et al, 2007). The study of DNA methylation is of particular importance in cancer, as causal involvement has been demonstrated and it is the most stable of all epigenetic modifications, making it a desirable marker for both early detection and treatment of tumors. Hypermethylation of CpG sites in gene promoter regions leads to decreased gene expression; if such a gene is a tumor suppressor, this leads to carcinogenesis. To date, there have been no studies of genome-wide DNA methylation profiling of NETs. This study sets out to determine the DNA methylation profiles of low, intermediate and high grade pancreatic NET liver metastases with the intention of identifying dysregulated biological pathways in the development of these tumors. A protocol for the analysis formalin-fixed paraffin embedded tissue (FFPE) has also been developed in order to study these tumors in significant numbers following this pilot study.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Dr Christina Thirlwell
#67 Interest of combined chromogranin A and pancreatic polypeptide for diagnosis and follow-up of gastroenteropancreatic endocrine carcinoma
Introduction: Assessment of tumor burden changes is essential for the management of well-differentiated gastroenteropancreatic neuroendocrine carcinoma (GEPNET). Chromogranin A (CgA) is the principal tumor marker for such tumors; however, its use to evaluate morphological tumor progression is not validated. Combined CgA and pancreatic polypeptide (PP) may increase sensitivity in the diagnosis of GEP-NET.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Dr Thomas WALTER
#81 Gastroenteropancreatic neuroendocrine tumors (GEP-NETs): our experience in a multidisciplinary team in a university hospital
Introduction: Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) have a low incidence and prevalence representing < 2% of all gastrointestinal tumors with a heterogeneous biological behavior and an often complex management.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Dr Jose Manuel Cabezas-Agricola
#83 Surgical treatment of duodenopancreatic neuroendocrine tumors (pNETs) in patients with multiple endocrine neoplasia type 1 (MEN 1): a Dutch consensus statement
Introduction: Duodenopancreatic neuroendocrine tumors (pNETs) in multiple endocrine neoplasia type 1 (MEN 1) are the most important cause of MEN 1-related death. Surgery is the only curative treatment, but controversy exists on the optimal strategy. Recent guidelines on pNETs have limited recommendations specific for MEN 1. Therefore, a Dutch multidisciplinary consensus meeting was organized.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD Carolina RC Pieterman
#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
Authors: Delektorskaya V, Chemeris G, ...
#106 Gastroenteropancreatic neuroendocrine tumors: single institution clinicopathological study
Introduction: Neuroendocrine cells are widely distributed throughout the body, and neoplasms from these dispersed cells can arise at many sites. They are distinguished into two broad categories: 1) Tumors identified as small cell lung carcinomas with biology and natural history of a high-grade malignancy and characteristics of small cell undifferentiated or anaplastic appearance by light microscopy. The WHO categorizes these tumors as poorly-differentiated neuroendocrine carcinomas; 2) Well-defined neuroendocrine tumors (NETs) with variable, but most lyindolent biologic behavior and characteristic well-differentiated histologic features. The majority arise in the gastrointestinal tract and collectively they are referred as gastroenteropancreatic neuroendocrine tumors (GEP/NETs). They include carcinoid tumors, pancreatic islet cell tumors (gastrinoma, insulinoma, glucagonoma, VIPoma, somatostatinoma), paragangliomas, pheochromocytomas, and medullary thyroid carcinomas. The WHO classifies the GEP/NETs as well-differentiated NETs (carcinoid tumors) if they are noninvasive and have benign behavior or uncertain malignant potential. In contrast, GEP/NETs with characteristics of low-grade malignancy with invasion of the muscularis propria or beyond, or metastases, are characterized as well-differentiated neuroendocrine carcinomas (malignant carcinoids). Pancreatic islet cell tumors, whether functioning or not, are classified as well-differentiated NETs or well-differentiated neuroendocrine carcinomas, due to the (depending on) histologic characteristics. The WHO classification for gastroenteropancreatic NETs based on stage (ie size and presence of metastases) and grade (mitotic rate, perineural and lymphovascular invasion, Ki-67 proliferative index) categorizes them as well-differentiated NETs, e.g., carcinoid tumors, or as well-differentiated neuroendocrine carcinomas.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Dr Michael M. Vaslamatzis
#127 Sunitinib for the treatment of advanced, progressive pancreatic neuroendocrine tumors
Introduction: Sunitinib is an oral, multitargeted tyrosine kinase inhibitor approved for use in advanced renal cell carcinoma and imatinib-resistant/intolerant gastrointestinal stromal tumors. Investigations of sunitinib in the RIP1-Tag2 mouse model and in phase I/II clinical trials provide evidence of antitumor activity against pancreatic neuroendocrine tumors (NET).
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Prof Eric Raymond
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