Abstract library

140 results for "drug resistance".
#1739 A Kinomic Approach to Identify Signaling Proteins Involved in Drug Resistance in GastroEnteroPancreatic Neuroendocrine Tumors
Introduction: Most of the current therapeutic strategies used for neuroendocrine tumors (NETs) result in tumour growth stabilization, eventually followed by tumour progression. Thus, despite their original characteristics, NETs exhibit similar resistance features to treatments than other more common tumours.
Conference: 14th Annual ENETS conference (2017)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Dr David Romano
#2091 Differential Signalling Pathways Drive Therapeutic Resistance in Neuroendocrine Tumors
Introduction: Most of the current therapeutic strategies used for neuroendocrine tumors (NETs) are insufficient due to poor knowledge of these tumours. Despite showing differentiated features, NETs often exhibit therapeutic resistance to common treatments similarly to other cancers. Although signalling abnormalities have been reported, molecular mechanisms responsible for this resistance phenomenon are yet to be understood.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Dr David Romano
Authors: Romano D, Gerard C, Poizat F, Niccoli P, ...
#2018 Ex Vivo Activity of Cytotoxic Drugs and Targeted Agents in Small Intestinal Neuroendocrine Tumors
Introduction: Small Intestinal Neuroendocrine Tumours (SI-NETs) are considered to be generally resistant to systemic treatment. To date predictive markers for drug activity are lacking.
Conference: 15th Annual ENETS conference (2018)
Category: Medical treatment - Chemotherapy Somatostatin analogues, Interferon
Presenting Author: Kosmas Daskalakis
#921 Combined Therapy with RAD001 e BEZ235 Overcomes Resistance of PET Cells to mTOR Inhibition
Introduction: Since the PI3K/Akt/mTOR proliferation axis is often deregulated in PETs, the mTORC1 complex inhibitor Everolimus (RAD001) represents an effective treatment for PETs. However, RAD001 leads to a re-activation of PI3K activity and phosphorylation of Akt, which may promote resistance to the treatment. Thus, direct inhibition of PI3K may represent a novel potential target for PETs.
Conference: 11th Annual ENETS Conference (2014)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Dr Gabriele Capurso
Keywords: mTOR, PI3K, resistance
#2287 Mitochondrial or Aerobic Glycolysis Oriented Metabolism May Define Pancreatic Neuroendocrine Tumors (PanNET) Resistance to mTOR-Targeting Therapies
Introduction: The mTOR inhibitor Everolimus is approved for the treatment of PanNET and no predictive biomarker is available. mTOR is a central node controlling mitochondrial and aerobic glycolytic metabolisms.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - Genetics, epigenetics, miRNAs, Omics
Presenting Author: Dr Jerome Cros
Authors: Cros J, Bucau M, Raffenne J, Soukeur M, ...
#55 Metronomic combination therapy including temozolamide, bevacizumab and somatostatin analogue for the treatment of malignant gastroenteropancreatic neuroendocrine tumors
Introduction: Malignant gastroenteropancreatic neuroendocrine tumors (GEPNETS), mainly carcinoids, are not considered to be particularly chemotherapy-sensitive to conventional chemotherapeutic schemes. Long-standing evidence suggests these tumors to be highly vascularised and responsive to antiangiogenic strategies. Newest reports demonstrate benefit by the use of temozolamide, an oral alkylating agent similar to intravenous dacarbazine. The DNA repair enzyme O6-alkylguanine–DNA alkyltransferase (AGAT) confers cancer cell resistance to O6-alkylating agents such as temozolamide through its ability to remove methyl/alkyl groups from the O6-position of guanine, thus correcting drug-induced DNA damage.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: DR Anna Koumarianou
#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
#2271 Effects of Multi-Receptor Targeting Drugs in Neuroendocrine Tumors Using 3D Cell Culture
Introduction: Symptom control in functioning neuroendocrine tumors(NETs) may be difficult in some cases, thus, new therapeutic options, including multi-receptor targeting drugs are required.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: Aura Dulcinea Herrera-Martínez
#1869 Synergistic Effects of Combining Hsp90 and PI3K Inhibitors with Everolimus in Pancreatic Neuroendocrine Tumors
Introduction: The development of the first molecular targeted therapies for neuroendocrine tumors (NET) was a milestone in the treatment of patient. Nevertheless, these therapies eventually fail and patients become resistant to the treatment. One way of escaping this dilemma might be the combination of targeted drugs to prevent resistance development.
Conference: 14th Annual ENETS conference (2017)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Dr Joerg Schrader
Authors: Weissmann V, Benten D, Fahl M, Eggers C, ...
#1999 Study of Cell Cycle Protein Expression Pattern in Bronchial Carcinoids: A New Potential Target for Medical Therapy?
Introduction: Bronchial Carcinoids (BCs) are rare neuroendocrine neoplasms arising from respiratory epithelium. The only effective treatment option is surgery, but its efficacy is frequently limited by metastatic spread. Everolimus prolongs progression free survival but patients may develop resistance. Previous studies demonstrated that Everolimus reduces viability of NCI-H720 cells (Atypical Carcinoid) but not of NCI-H727 cells (Typical Carcinoid). Everolimus decreases Ciclyn D1 protein levels in both cell lines but NCI-H727 cells survive, indicating a derangement in cell cycle control.
Conference: 15th Annual ENETS conference (2018)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Giulia Bresciani
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