Abstract Library
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ENETS Abstract Search
Introduction: Gastric mixed adenoneuroendocrine carcinomas (g-MANECs) are rare neoplasms consisting of adenocarcinoma and neuroendocrine neoplastic components. G-MANECs show more malignant characteristics than gastric adenocarcinomas, while molecular mechanisms underlying the co-existence of the two components remains unknown.
Conference: 17th Annual ENETSConcerence (2020)
Presenting Author:
Authors: Yan S, Chen X, Zhang R, Song L, Yin F,
Keywords: whole exome sequencing, mixed adenoneuroendocrine carcinoma, Stomach, Evolution,
#2804 Claudin-18 Is a Sensitive and a Specific Marker for Gastric Neuroendocrine Tumors
Introduction: Antibody-based cancer therapies are emerging as promising therapeutics in oncology, including one in clinical trials that targets claudin-18, a protein expressed in normal gastric epithelium and some gastric adenocarcinoma. We currently have no markers for gastric well-differentiated neuroendocrine tumors (NETs).
Conference: 17th Annual ENETSConcerence (2020)
Presenting Author:
Authors: Wong M, Huynh C, Kim S, Dhall D, Guindi M,
Keywords: claudin-18, anti-claudin 18, neuroendocrine tumor, neuroendocrine hyperplasia, autoimmune metaplastic atrophic gastritis,
Introduction: The outcome of the gastric neuroendocrine carcinoma (GNEC) was poor. However, there was few studies analyze the difference of long-term outcomes after radical surgery between GNEC and gastric adenocarcinoma (GAC).
Conference: 14th Annual ENETSConcerence (2017)
Presenting Author: Jian-Wei X
Authors: Jian-Wei X, Chao-Hui Z, Ping L, Jia-Bin W, Jian-Xian L,
Keywords: Gastric neoplasm, Neuroendocrine neoplasm, Prognosis, Propensity score matching study,
Introduction: Autoimmune gastritis (AIG) causes oxyntic gland atrophy. This condition is often associated with Type-1 gastric NET secondary to achlorhydria and hypergastrinemia. Similar to atrophic gastritis in non-autoimmune conditions, AIG is associated with intestinal metaplasia that could progress to glandular dysplasia.
Conference: 9th Annual ENETSConcerence (2012)
Presenting Author:
Authors: Tang L,
Keywords: Type-I gastric NET, gastric adenocarcinoma,
#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 ENETSConcerence (2010)
Presenting Author: Francis de Oliveira Alves
Authors: Caponero R, Francis de Oliveira Alves , Flávio Issao Sakamoto , Osmar Martins Cruz Jr. ,
Keywords: gastric carcinoid tumors type 1, octreotide LAR, ECLomas, neuroendocrine tumors,