Abstract library

130 results for "New release mechanism".
#2087 Prospective, Multi-Center, Open Label, Phase Study II of APOC, a New Controlled Release 15mg Octreotide Acetate, for the Treatment of Advanced NETs
Introduction: Somatostatin analogues (SSAs) are the cornerstone of systemic therapy of advanced NETs. The efficacy controlling hormone release and tumor growth together with the favorable toxicity profile have positioned SSAs as upfront therapy. Despite of second-line therapies including targeted agents, chemotherapy and radiolabeled peptides have demonstrated activity controlling tumor growth, the less favorable toxicity profiles become a usual discussion with patients (pts) to preserve the quality of life (QoL). Additionally, from concordant flow of evidences clinical benefits could be obtained with higher SSAs circulating levels but remain unreachable with current products. APOC is a new controlled release ready-to-use convenient therapeutic, designed to cover specifically these clinical unmet needs.
Conference: 15th Annual ENETS conference (2018)
Category: Medical treatment - Chemotherapy Somatostatin analogues, Interferon
Presenting Author: Dr Jaume Capdevila
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#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
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#2081 Preclinical Testing of SSA Compounds in a Model of Pancreatic Neuroendocrine Tumors to Optimize Scheduling and Drug Exposition
Introduction: Somatostatin analogues (SSA) such as Octreotide and Lanreotide have demonstrated a significant benefit in Neuroendocrine Tumors, particularly in the well/moderately differentiated types. Nevertheless, there are still several aspects of SSA treatments that remain unsolved, such as drug exposition in patients and schedule optimization.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: PhD Oriol Casanovas
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#1467 iFiT: An Integrative Bioinformatics Platform for Biomarker and Target Discovery. A Case Study in Neuroendocrine Tumors
Introduction: iFiT (Ipsen Focused-on-new bIological enTities and biomarkers) is a Bioinformatics platform integrating systems biology functionalities together with semantic & logic-based artificial intelligence within a high-scale computing environment.
Conference: 13th Annual ENETS conference (2016)
Category: Biomarkers
Presenting Author: PhD Sebastien Tourlet
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Keywords: Targets iFiT
#2075 Phase 1 Pharmacokinetic and Pharmacodynamic Study of APOC, a New Controlled Release Formulation (CRF) of 15mg Octreotide Acetate in Healthy Male Volunteers
Introduction: Somatostatin analogues (SSAs) are considered the gold standard for systemic therapy of advanced neuroendocrine tumors (NETs). Octreotide is one of the SSAs most widely used in long-term therapies of NETs. There is increasing evidence that clinical benefits could be obtained with higher SSAs circulating levels but remain unreachable with current products without impacting significantly the quality of life of the patients. APOC is a new injectable controlled release technology containing Octreotide invented and developed by Ascil-Biopharm and designed to cover specifically these clinical unmet needs. It is presented as ready-to-use and can easily be manufactured at selected doses and durations in prefilled syringe.
Conference: 15th Annual ENETS conference (2018)
Category: Medical treatment - Chemotherapy Somatostatin analogues, Interferon
Presenting Author: Rosa Maria Antonijoan Arbós
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#1111 Autophagy as a Possible Mechanism of Resistance in pNET Treatment
Introduction: Pancreatic neuroendocrine tumor (pNET) patients often display primary or secondary resistance to Sunitinib, an anti-angiogenic multi-receptor tyrosine kinase inhibitor which has been approved for the treatment of late stage pNETs. In late cancer stage autophagy often has a tumor promoting role. Sunitinib might additionally activate autophagy through inhibition of mTOR or induction of hypoxia.
Conference: 12th Annual ENETS Conference (2015)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Tabea Wiedmer
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#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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#204 A Proteomic Approach Identifies Novel Proteins Involved in Invasion Mechanisms in Enteroendocrine Carcinomas
Introduction: Enteroendocrine tumors dramatically lack reliable biomarkers to accurately select therapeutic strategy, due to a poor knowledge of molecular mechanisms leading to local invasion and dissemination.
Conference: 8th Annual ENETS Conference (2011)
Category: Basic
Presenting Author: Colette Roche
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#458 Octreotide Long-Acting ReleaseTherapy for Patients with Functional and Metastatic Gastroenteropancreatic Neuroendocrine Tumors: A Retrospective Analysis in Chang-Gung Memorial Hospital
Introduction: Reports of octreotide therapy for symptomatic control in patients with functioning gastroenteropancreatic neuroendocrine tumors (GEP-NETs) in Asia are lacking.
Conference: 9th Annual ENETS Conference (2012)
Category: Clinical
Presenting Author: Dr. Chia-Hsun Hsieh
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#527 Pheochromocytoma Molecular Analysis After Maternal Transmission of SDHD Mutation Elucidates Mechanism of Parent-of-Origin Effect
Introduction: In SDHD mutation families, paragangliomas and pheochromocytomas usually occur only after paternal transmission of the mutation. This important but unexplained parent-of-origin effect is not due to imprinting of the SDHD gene itself (as was initially suspected) since SDHD is biallelically expressed.
Conference: 9th Annual ENETS Conference (2012)
Category: Basic
Presenting Author: Dr Edward Tobias
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