Abstract library

1752 results for "tumor size".
#1803 Type 3 Gastric Neuroendocrine Neoplasms: Relationship Between Tumor Size, Ki67 and Clinical Outcome
Introduction: Sporadic type 3 gNENs are usually malignant with high metastatic potential, mostly large, with a high grade histology. However, little is known on the relationship between tumor size, proliferative index Ki67, and clinical outcome
Conference: 14th Annual ENETS conference (2017)
Category: Epidemiology/Natural history/Prognosis - Prognosis
Presenting Author: Dr. Francesco Panzuto
#296 Tumor Size Correlates With Malignancy in Non-Functioning Pancreatic Endocrine Tumor
Introduction: Tumor size is a criterion of staging in non-functioning pancreatic endocrine tumors (NF-PET), as well as a predictor of outcome after curative resection.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: MD Massimo Falconi
#2200 Tumor Size Correlates with Grading in Nonfunctioning Pancreatic Neuroendocrine Tumors and Is Not Age-Dependent
Introduction: Tumor growth and Ki67 value increase are associated with aggressiveness in nonfunctioning pancreatic neuroendocrine tumours (NF-PanNET), but their natural history is largely unknown. It is unknown if the evolution of NF-PanNET is time-dependant.
Conference: 15th Annual ENETS conference (2018)
Category: Surgical treatment and Ablative Therapies
Presenting Author: Francesca Muffatti
#19 Antitumor activity of Pasireotide (SOM230) alone and in combination with Everolimus (RAD001) in DU-145 human prostate cancer model
Introduction: Pasireotide (SOM230) is a novel multi-receptor ligand somatostatin analogue with high affinity for somatostatin receptor subtypes sst1,2,3 and sst5. Like octreotide, which binds primarily to sst2, it inhibits hypersecretion of hormones from patients with functional pituitary tumors and gastroenteropancreatic neuroendocrine (GEP/NET) tumors. In addition, tumor shrinkage has been observed with both compounds in patients with acromegaly, Cushing’s disease and GEP/NETs, but its tumor-reducing mechanism of action has so far not been revealed. In patients with breast and liver cancer, octreotide had little or no antitumor activity.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Dr. Herbert A. Schmid
Authors: Schmid H A, Chiara L, Nuciforo P, ...
#108 Everolimus (RAD001) induces tumor response in patients with medullary thyroid cancer: an in vivo and in vitro study
Introduction: Medullary thyroid cancer (MTC) is a neuroendocrine tumor (NET) of the thyroid C cells which is known to express somatostatin receptors. Octreotide, a somatostatin analogue exerting both antisecretory and antitumor activity in different types of NETs, has shown low efficacy in MTC. Everolimus (RAD001), an inhibitor of mTOR, has shown antitumor effects in patients with NETs and synergistic effects when combined with octreotide. Until recently, RAD001 has never been evaluated in MTC.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: MD, PhD Antongiulio Faggiano
#1479 Comparison of Radiological and Histological Tumor Size in Pancreatic Neuroendocrine Neoplasm
Introduction: Radiological tumor size of pancreatic neuroendocrine neoplasms (PNEN) is crucial for management especially for asymptomatic, small lesions.
Conference: 13th Annual ENETS conference (2016)
Category: Surgical treatment
Presenting Author: Stefano Partelli
#203 Liver and Liver-Pancreastransplantation in the Two-stage Treatment of Liver Metastasized Neuroendocrine Tumors of the Pancreas: About Three Cases
Introduction: Although liver transplantation is a valid option in the treatment of metastasized neuroendocrine tumors, it is not promoted because of a donor organ shortage and disappointing results in older series.
Conference: 8th Annual ENETS Conference (2011)
Category: Clinical
Presenting Author: Dr. Geert Roeyen
#2051 Do We Need Hormonal Therapy for Pancreatic Neuroendocrine Tumors? An Effort to Reduce the Size of PanNETs
Introduction: Pancreatic neuroendocrine tumors although rare , have been significantly increased over the past few decades. They range from indolent to highly aggressive in nature. Just like breast and endometrial carcinoma are hormonal dependant,
Conference: 15th Annual ENETS conference (2018)
Category: Medical treatment -Targeted therapies
Presenting Author: Dr Arooj Fatima
Authors: Fatima A, Zaidi S S A, ...
#724 Contrast-Enhanced Ultrasonography (CEUS) Reliably Predicts Tumor Progression in Pancreatic Neuroendocrine Tumors
Introduction: Neuroendocrine tumors (NETs) exhibit a typical vascular pattern in the arterial phase on CEUS. The role of CEUS in the prognostic evaluation of pancreatic NET (pNET) has been poorly investigated.
Conference: 10th Annual ENETS Conference (2013)
Category: Imaging (radiology, nuclear medicine, endoscopy)
Presenting Author: Michela Del Prete
#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
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