Abstract library

658 results for "enterochromaffin-like cell hyperplasia".
#3004 Development of Anti-SSTR CAR T Cells for Future Treatment of NETs
Introduction: NETs overexpress somatostatin receptors (SSTRs).
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: Dr. Mauro Cives
#3084 Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH): A Case Report and Review of Literature
Introduction: Majority of euroendocrine tumorsare found in the gastrointestinal tract and bronchopulmonary. Multifocal disease is common among patients with low-grade NET. One example of this is diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. DIPNECH is an extremely rare but indolent disease with predilection for nonsmoking, middle-aged women.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Case reports
Presenting Author: Dr Mary Anne Cruz
Authors: Cruz M A, ...
#2739 Epigenetic Landscape of Pancreatic Neuro-Endocrine Tumors Reveals Distinct Cells of Origin and Means of Tumor Progression
Introduction: Pancreatic Neuroendocrine Tumors (PanNETs) arise from cells of the Islets of Langerhans. The majority of PanNETs are non-functional and their cell of origin cannot be defined analysing specific hormone production. Cell of origin assessment has proven importance to identify risk factors, prevent tumour development, and tailor treatment in many malignancies. Recent data on super-enhancer signatures has suggested a potential origin of PanNET from α- or β-cells. We and others have shown that distinct epigenetic profiles assessed by DNA methylation (DNAme) characterize genomic and prognostic groups of PanNET.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: Annunziata Di Domenico
#2754 Somatostatin Analogs (SSA) in Patients with Symptomatic Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH)
Introduction: DIPNECH is characterized by a proliferation of pulmonary neuroendocrine cells and multifocal neuroendocrine tumorlets and/or tumors. Although usually indolent, DIPNECH can cause chronic cough and dyspnea. There is very limited information on treatment.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Medical treatment - Chemotherapy Somatostatin analogues, Interferon
Presenting Author: Dr. Jonathan Strosberg
#2980 Metabolic Dysregulation and Circadian Clock in Cellular Models of Neuroendocrine Tumors
Introduction: The circadian clock genes encode transcription factors whose interaction with nuclear receptors allows the regulation of cellular metabolism.The invalidation of the genes of the clock core is associated with the development of many endocrine diseases including neuroendocrine cancer. Recently, the family of transcriptional coactivators PGC-1a has been identified as a key element in the integration of cellular metabolic state with the circadian clock. PRC, as a member of the PGC-1 family, was able to interact with several transcription factors, including the CLOCK factor. The specific induction of this PRC factor by the cell cycle, to modulate the energy function, the MAPkinase pathway and the expression of microRNAs, makes it a key factor in the metabolic adaptation of cancer cells.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Pr Frederique Savagner
Authors: Savagner F, Le Pennec S, ...
#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
#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, ...
#830 The Predictive Value of Gastrin Levels for the Diagnosis of Gastric Enterochromaffin-like Cells Hyperplasia, in Patients with Hashimoto’s Thyroiditis
Introduction: Gastrin and chromogranin A (CgA) levels have been tested for the diagnosis of enterochromaffin-like cell hyperplasia (ECLH), in patients with type 1 diabetes and autoimmune atrophic gastritis but there are no data for patients with Hashimoto's thyroiditis (HT).
Conference: 11th Annual ENETS Conference 2014 (2014)
Category: Biomarkers
Presenting Author: Dimitrios Thomas
#3049 Organoid Models of Neuroendocrine Cell Growth and Tumorigenesis
Introduction: A paucity of in vitro and in vivo models has limited the study of Neuroendocrine neoplasms (NENs). Moreover, little is known about normal neuroendocrine (NE) cells and how they contribute to NEN formation.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: PhD Talya Dayton
#3005 Comparison between Tang and WHO 5th Edition Grade Classification for Goblet Cell Adenocarcinomas
Introduction: Appendiceal GCAs (previously Goblet Cell Carcinoids) are composed of cells with secretory phenotypes. Several grading systems to predict behaviour are available (e.g.Tang). The latest WHO 5th edition adopted a grading system similar to colon adenocarcinomas.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Pathology - grading, staging
Presenting Author: MD, PhD Jorge Barriuso