Abstract library

1616 results for "gastric carcinoid tumors type 1".
#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
#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, ...
#184 Somatostatin Analogues as a Therapeutic Option in a Series of 91 Patients with Gastric Carcinoids
Introduction: Gastric carcinoid tumors (GC) represent about 10-30% of carcinoid tumors and about 1% of all stomach neoplasms. They include three types : type 1 (70-85%), type 2 (5-10%) and type 3 (15-25%).
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: MD Christos St. Basagiannis
#190 Complete Remission in a Patient with Metastatic Type 1 Gastric Carcinoid (GCA1) Treated with a Long-acting Somatostatin Analogue
Introduction: Surgery is the treatment of choice for invasive and metastatic GCA1. Somatostatin analogues have been successfully used in GCA1 patients without signs of malignancy.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Dr merav Fraenkel
#295 Unusual Behavior of Gastric Carcinoid Type 1
Introduction: Gastric carcinoids (GC) are rare tumors of the stomach. GC type 1 are associated with chronic atrophic gastritis (CAG) and are the most benign type, having low metastatic potential.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Matilde P Spampatti
#406 YF476, a Gastrin Receptor Antagonist, Causes Regression of Tumors and Normalizes Serum Chromogranin A in Patients with Type 1 Gastric Carcinoids
Introduction: Chronic atrophic gastritis (CAG) results in achlorhydria, hypergastrinemia and, in some patients, gastric carcinoids (type 1 GCs). Type 1 GCs may become malignant and metastasize. Current treatments of type 1 GCs, such as polypectomy, somatostatin analogues and antrectomy, have their disadvantages. YF476 – a potent, selective, orally active and well-tolerated gastrin receptor antagonist in pre-clinical studies – prevented, as well as reduced, the number and size of gastric carcinoids and carcinomas in rodent models.
Conference: 9th Annual ENETS Conference (2012)
Category: Clinical
Presenting Author: Reidar Fossmark
#763 Endoscopic Therapy with Argon Plasma Coagulation for Multiple Type 1 Gastric Carcinoid Tumors
Introduction: Data regarding Type I gastric carcinoids and their evolution in prospective series are scarce, thus treatment and follow-up are not codified.
Conference: 10th Annual ENETS Conference (2013)
Category: PRRT-Ablative therapies-Endoscopic treatment
Presenting Author: Dr. Rodrigo Castano
#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
#802 Metastatic Type 1 Gastric Carcinoid - A Real Threat or Just a Myth?
Introduction: Metastatic GCA1 are extremely rare and there is no data about their natural history, treatment and prognosis.
Conference: 11th Annual ENETS Conference (2014)
Category: ...none of the below
Presenting Author: Dr. Simona Glasberg