Introduction: Typical bronchial carcinoids (TBC) are well-differentiated neuroendocrine neoplasms (NEN) whose management can still be very challenging due to reduced sensitivity to therapy. Previous studies have reported TGF-β’s ability to activate mTOR pathway and induce epithelial to mesenchymal transition (EMT). Moreover, preliminary results show an overexpression of TGF-β signalling and caspase activation in TBC.
Conference: 18th Annual ENETS Conference 2021 (2021)
Category: Basic science - Signalling pathways, receptors, biomarkers
Presenting Author: Patricia Borges de Souza
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)
Presenting Author: MD Ricardo Caponero
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)
Presenting Author: MD, PhD Apostolos Tsolakis
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)
Presenting Author: Reidar Fossmark
Introduction: The actual incidence of type1 gastric carcinoids (GC1) as a long-term complication of chronic autoimmune atrophic gastritis (CAAG) remains to be clarified as studies are few.
Conference: 10th Annual ENETS Conference 2013 (2013)
Category: Non digestive NETs (bronchial, MTC, pheochromocytoma)
Presenting Author: Dr Roberta E Rossi