Abstract library

1889 results for "digestive neuroendocrine tumors".
#1675 Abdominal Obesity, Fasting Glucose and Metabolic Syndrome Are Risk Factors for Well Differentiated Digestive Neuroendocrine Tumors
Introduction: Digestive NETs(DNETs)`s incidence has increased last 40 years. Visceral obesity and metabolic syndrome (MetSyn) were recently reported to be associated with several cancers, although not so far with DNET.
Conference: 14th Annual ENETS conference (2017)
Category: Epidemiology/Natural history/Prognosis - Descriptive epidemiology
Presenting Author: Dr. Ana Paula Santos
#1124 Correlation Between the 18F-FDG Uptake and Pathological Data in Well-Differentiated Digestive and Pulmonary Neuroendocrine Tumors (NET)
Introduction: The 18F-FDG uptake assessed by PET/CT is correlated to prognosis in most tumors.
Conference: 12th Annual ENETS Conference (2015)
Category: Pathology, grading, staging
Presenting Author: Margot Bucau
#11 Plasma chromogranin - A response to octreotide test: Prognostic value for clinical outcome in endocrine digestive tumors
Introduction: Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) expressing somatostatin receptors may be treated with somatostatin analogues (SSAs). Selection criteria are a positive Octreoscan® or a >50% hormone level decrease after octreotide s.c. injection (octreotide test) (OT). Plasma chromogranin A (CgA) is the best general GEP-NET marker, but data on CgA response to OT are scant.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD, PhD Sara Massironi
#1387 FOLFOX in Neuroendocrine Tumors
Introduction: Favorable toxicity profile and significant antitumor activity of FU-oxaliplatin in several malignancies led us to evaluate FOLFOX in advanced neuroendocrine carcinomas (NETs).
Conference: 13th Annual ENETS conference (2016)
Category: Medical treatment - Chemotherapy
Presenting Author: Marjorie Faure
Authors: Faure M, Raoul J L, Autret A, Mineur L, ...
#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
#297 Hepatic Arterial Embolization v. Chemoembolization in Patients with Liver Metastases of Digestive Neuroendocrine Tumors
Introduction: Promising results have been reported using hepatic arterial chemoembolization (CE) or embolization (E) alone in patients with liver metastases of DET, but these modalities have not been compared.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Pr Philippe Ruszniewski
#867 Mixed Adenoneuroendocrine Carcinoma (MANECs): A Rare and Challenging Subgroup of Neuroendocrine Neoplasia
Introduction: Mixed Adenoneuroendocrine Carcinomas (MANECs) are rare entities in which at least 30% of neoplastic cells are neuroendocrine in nature (WHO 2010 classification). They result either from two independent lesions that merge together or are unique lesions with different cell populations intermingled.
Conference: 11th Annual ENETS Conference (2014)
Category: Pathology, grading, staging
Presenting Author: Dr Conor Mosli Lynch
#682 Neuroendocrine Tumors, Searching for New Prognostic Biomarkers
Introduction: Neuroendocrine tumors (NET) of the digestive system were once considered relatively rare, however, the incidence is increasing. New prognostic biomarkers are needed for assessment of tumor behavior to inform patient treatment and improve outcome. The proliferation marker, Ki-67, is used for NET grading. Although classified as low grade, some tumors actually develop metastases.
Conference: 10th Annual ENETS Conference (2013)
Category: Biomarkers
Presenting Author: Helen Miller
#2015 Single-Institutional Review of Non-Pancreatic GI Neuroendocrine Tumors
Introduction: Neuroendocrine tumors (NETs) most commonly occur in the digestive tract with an incidence of 3.56 per 100,000 with 94% of those being non pancreatic.
Conference: 15th Annual ENETS conference (2018)
Category: Epidemiology/Natural history/Prognosis- Registries, nationwide and regional surveys
Presenting Author: M.D. Alaa El Chami
#2250 Treatment Outcomes of Patients with Mixed Neuroendocrine Non-Neuroendocrine Neoplasms (MiNEN)
Introduction: Mixed neuroendocrine non-neuroendocrine neoplasms (MiNEN) have been newly defined in the WHO 2017 classification. They are rare tumors, commonly treated in analogy to their non-neuroendocrine (nNE) or neuroendocrine (NE) component without systematic data regarding the optimal therapeutic strategy.
Conference: 15th Annual ENETS conference (2018)
Category: Epidemiology/Natural history/Prognosis- Registries, nationwide and regional surveys
Presenting Author: Dr. med. Leonidas Apostolidis