Abstract library

317 results for "chromogranin A secretion".
#1476 Efficacy of Everolimus and Somatostatin Analogs as Single Agents or in Combination in Human Pancreatic Neuroendocrine Tumors Primary Cultures
Introduction: Among the therapeutic options available for the treatment of neuroendocrine tumors, one targeted therapy, everolimus (RAD) has been approved for advanced progressive pancreatic neuroendocrine tumors (pNETs). It improve progression free survival but is not curative. Alterations of the PI3K/Akt/mTOR pathway in pNETs have given the rational for the use of this signaling pathway inhibitors.
Conference: 13th Annual ENETS conference (2016)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: doctor Corinne Gerard
#1543 Is True Non-Secretion of Chromogranin A an Unfavorable Prognostic Factor in Patients with ENETs TNM Stage IV Gastroenteropancreatic Neuroendocrine Tumors?
Introduction: Chromogranin A (CgA) is the best available serum marker for the work-up of gastroenteropancreatic NETs (GEP-NETs) and correlates with tumor volume & biological activity. During diagnosis & follow-up we found patients with elevated CgA levels and patients without elevated CgA levels (=‘true non-secretors’). We postulated that lack of secretion is a sign of dedifferentiation with a poorer prognosis.
Conference: 13th Annual ENETS conference (2016)
Category: Biomarkers
Presenting Author: drs. Kimberly Kamp
Keywords: GEP-NET, CgA, prognosis
#2219 24 Hour Urinary 5-Hydroxyindoleacetic Acid Levels in Patients with Non-Functioning Pancreatic Neuroendocrine Tumors
Introduction: The secretion of urinary 5-Hydroxyindoleacetic Acid (u5-HIAA) by non-functioning PNETs (NF-PNET) has rarely been reported, and the data on the association between u5-HIAA levels and disease burden is scant.
Conference: 15th Annual ENETS conference (2018)
Category: Biomarkers
Presenting Author: Dr Amit Tirosh
#532 Effect of the Combined Administration of mTOR Inhibitor and Dopamine or Somatostatin Analogues in a Human Bronchial Neuroendocrine Cell Line
Introduction: The mTOR inhibitor rapamycin (RAP) has been considered an anticancer agent. The role of dopamine and somatostatin in controlling cell secretion and proliferation in neuroendocrine tumors (NETs) is still unclear.
Conference: 9th Annual ENETS Conference (2012)
Category: Basic
Presenting Author: Prof Rosario Pivonello
#1917 Clinical Correlates of Discrepant Results of Chromogranin a versus Serotonin Markers in Patients with Neuroendocrine Tumors
Introduction: Neuroendocrine tumors lead to elevated chromogranin A levels and elevated serotonin markers (urinary 5HIAA and platelet serotonin). These markers are employed for diagnosis and monitoring.
Conference: 14th Annual ENETS conference (2017)
Category: Biomarkers
Presenting Author: Dr Wim Meijer
Authors: Meijer W, Bruikman C, Beukeveld G, ...
#2245 Metastatic VIPOMA, Co-Secreting Insulin, with Complete Response to Lanreotide Combined with Capecitabine and Temozolamide
Introduction: VIPomas are rare neuroendocrine tumors (NETs) associated with vasoactive intestinal polypeptide (VIP) hypersecretion causing watery diarrhea, hypokalaemia and achlorhydria. They originate mostly in the pancreas and 60-80% are malignant. Hormonal co-secretion is rarely reported.
Conference: 15th Annual ENETS conference (2018)
Category: Case reports
Presenting Author: Bernardo Marques
#2233 Potential Effects of Ketoconazole on ACTH-Producing and Non-ACTH-Producing Neuroendocrine Tumors
Introduction: Prolonged biochemical remission after treatment with steroidogenesis inhibitors has been described in patients with Cushing’s syndrome due to ectopic adrenocorticotropin hormone (ACTH) production. Some studies have suggested antiproliferative and apoptotic effect of ketoconazole in human cancer cells.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: Aura Dulcinea Herrera-Martínez
#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
#255 The Carcinoid Syndrome Caused by Retroperitoneal Carcinoid Tumors
Introduction: The carcinoid syndrome is caused by increased levels of serotonin and is mostly seen in cases of carcinoid tumor in the small bowel and liver metastases, as there is a very high first pass effect.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Dr Benedicte V Wilson
Authors: Wilson B, Nielsen H O, ...
#265 A Novel PKCßII Inhibitor Induces Antiproliferative Effects in Human Pancreatic Neuroendocrine Tumor Cells
Introduction: Deregulation of the protein kinase C (PKC) signaling pathway has been implicated in tumor progression.
Conference: 8th Annual ENETS Conference (2011)
Category: Basic
Presenting Author: MD Maria Chiara Zatelli