Gastroenteropancreatic neuroendocrine tumors (GEP-NETs): our experience in a multidisciplinary team in a university hospital Abstract #81

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.
Aim(s): To present our experience as a multidisciplinary team since its creation in April 2007.
Materials and methods: We conducted a prospective analysis of the patients seen in our team (n=35) from April 2007 to December 2009 (31 months). We analyzed separately pancreatic (PT) and extra-pancreatic tumors (exPT).
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Dr Jose Manuel Cabezas-Agricola

To read results and conclusion, please login ...

Further abstracts you may be interested in

#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
#18 Long-acting release octreotide induce complete response in type 1 gastric carcinoid tumors
Introduction: Gastric endocrine tumors (GET) are increasingly recognized due to expanding indications of upper gastrointestinal endoscopy. Often silent and benign, GET may also be aggressive when sporadic and may sometimes mimic the course of gastric adenocarcinoma. Current incidence of GETs is estimated at around 8% of digestive endocrine tumors. Yearly age-adjusted incidence is around 0.2 per population of 100,000. Gastric carcinoids (ECLomas) develop from gastric enterochromaffin-like cells (ECL cells) in response to chronically elevated gastrin. Type 1 tumors (ECLomas in the course of atrophic gastritis) may occur in conditions of achlorhydria secondary to auto-immune atrophic fundic gastritis. It occurs mostly in women and they are non-functioning tumors, typically found during upper GI endoscopy performed for dyspepsia. ECLomas present frequently as multiple polyps, usually < 1 cm in diameter in the gastric fundus. Type 1 tumors are almost exclusively benign lesions with little risk of deep invasion of the gastric parietal wall. The neoplastic ECL cells become progressively dedifferentiated with an increasing number of Ki-67 immunoreactive (IR) cell nuclei. In addition, there is a substantial decrease in argynophil and IR NE cells that can be visualized by conventional methods. ECLomas secondary to hypergastrinemia should be closely followed for signs of clinical and histopathological tumor progression. Such ECLomas deserve early, active, radical surgical treatment.
Traditionally, gastric carcinoid type 1 (GCA1s) are endoscopically or surgically removed, depending on the number, appearance and size of the tumors. Antrectomy, with surgical excision of the majority of the G cells, is thought to facilitate regression of these tumors by removing the source of excessive gastrin secretion; however, the long-term benefits of antrectomy still remain uncertain. Although proton pump inhibitors are effective in reducing hypergastrinemia-induced gastric acid hypersecretion in GCA2, they do not affect ECL-cell hyperplasia, and therefore their role in GCA1 is limited. Moreover, in selected cases, significant reduction of hypergastrinemia does not prevent development of ECL carcinoid, suggesting that, in addition to hypergastrinemia, other pathogenic or genetic factors may be involved. Treatment with somatostatin analogues (SSA) might impede ECL-cell hyperplasia by suppressing gastrin secretion and/or by a direct anti-proliferative effect on ECL cells. Treatment with SSAs in GCA1 leads to a substantial tumor load reduction, with a concomitant decrease of serum gastrin levels. Published data indicate an important anti-proliferative effect of SSA on ECL cells, providing clinical benefit and obviating, at least temporarily, the need for invasive therapies for GCA1. Morphometric studies demonstrated that, while antrectomy specifically decreased the volume of ECL cells versus the total volume of endocrine cells, octreotide reduces the overall endocrine cell volume. Although the number of treated patients is small, it has been suggested that SSA may exert important anti-proliferative effects either directly, by inhibiting ECL-cells proliferation, or indirectly through suppression of gastrin hypersecretion.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD Ricardo Caponero
#35 Primary Hyperparathyroidism in patients with gastric carcinoid Tumors type-1: an unusual coexistence
Introduction: Although a number of familiar endocrine syndromes are associated with primary hyperparathyroidism (PHP), there is no information regarding its prevalence in other sporadic neuroendocrine diseases.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Dr Dimitrios Thomas
#41 Immunohisochemical evaluation of EMT regulators, E- and N-cadherin in neuroendocrine Tumors of the Gastro-Entero-Pancreativ system
Introduction: Local tumor invasion represents the first step of the metastatic cascade of carcinomas, and requires changes in cell adhesion and migration properties of tumor cells. This biologic process is known as epithelial-mesenchymal transition (EMT). One key biochemical change associated with EMT is the loss of E-cadherin expression promoted by specific transcriptional repressors such as Snail, Slug, and Twist. Overexpression of EMT inducers increases other factors, such as FoxC2, although its role in EMT is poorly understood. Neuroendocrine tumors (NETs) of the gastroenteropancreatic (GEP) system, originated from the diffuse endocrine system, represent a heterogeneous group of tumors. Their prevalence has increased substantially over the past three decades, without substantial improvements in their clinical management, and their variable clinical course cannot be predicted by common clinicopathological parameters. Thus, new prognostic markers are urgently needed.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: JOSE A. GALVÁN
#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