Abstract library

21 results for "hypoxia".
#246 SDHB Loss Predicts Malignancy in Pheochromocytomas/Sympathethic Paragangliomas, but Not Through Hypoxia Signalling
Introduction: To date there is no reliable histopathological marker of malignancy for pheochromocytomas/sympathetic paragangliomas (PCC/PGL). It is well-known that PCC/PGL in the hereditary context of an SDHB germline mutation very often metastasize. The immunohistochemical loss of SDHB expression was recently shown to be a surrogate marker for the presence of an SDH germline mutation in PCC/PGL. SDHB loss is supposed to be tumorigenic via activation of hypoxia signals.
Conference: 8th Annual ENETS Conference (2011)
Category: Basic
Presenting Author: Dr Anja M Schmitt
#205 Integrated Genome-Wide DNA Methylation and mRNA Expression Analysis of Pancreatic NETs Identifies Differential Activation of the Hypoxia Inducible Factor (HIF) Pathway Between Low and Intermediate Grade Tumors
Introduction: This is the first study to integrate DNA methylation and mRNA expression analysis in NETs. It is a powerful approach with which to identify disrupted biological pathways in NET pathogenesis.
Conference: 8th Annual ENETS Conference (2011)
Category: Basic
Presenting Author: Dr Christina Thirlwell
#969 Identification of Hypoxia Induced Epigenetic Changes in the Development of Pancreatic Neuroendocrine Tumors
Introduction: In VHL syndrome, pancreatic NETs develop through bi-allelic inactivation of VHL with subsequent HIF pathway activation. This also occurs in sporadic pancreatic NETs.
Conference: 11th Annual ENETS Conference (2014)
Category: Basic Science - Genetics, epigenetics, miRNAs
Presenting Author: Dr Harpreet K Dibra
#466 HIF-1a Determines the Metastatic Potential of the GEP-NET Cell Line BON-1
Introduction: Intratumoral hypoxia is a hallmark of solid tumor formation and a negative predictor of patient survival. Adaptation to hypoxia is mainly achieved by the transcription factor HIF-1a, which is upregulated in a diverse range of human and experimental tumors and their metastases. HIF-1a target genes have been implicated in the induction of invasion and metastasis. However, HIF-1a’s tumor-supporting action depends on cell type and microenvironment and the precise role of HIF-1a for the pathogenesis of neuroendocrine tumors (NET) is largely unknown.
Conference: 9th Annual ENETS Conference (2012)
Category: Basic
Presenting Author: Katja Freitag de Molina
#99 Gene mutations and Hypoxia Inducible Factor (HIF-1) expression as prognostic-predictive factors in pheochromocytomas/paragangliomas (P/P)
Introduction: P/P are rare tumors sporadically associated with familial disorders. In advanced/unresectable disease, no standard treatment has so far been well established. Recently a mutation of some genes (SDHB, SDHC, SDHD) involved in the pathogenesis of familial P/P was discovered. These mutations are often associated with an over-expression of HIF-1, which plays a central role in angiogenesis and cell proliferation. This pathway is known to be inhibited by some targeted therapies, such as sunitinib or sorafenib.
Conference: 7th Annual ENETS Conference (2010)
Category: Basic
Presenting Author: Emilio Bajetta
#362 Succinate Dehydrogenase (SDH) Complex Expression in Pancreatic Endocrine Tumours (PETs)
Introduction: Absence of SDH subunit D (SDHD) mutations were reported by Perren et al (Oncogene 2002) but loss of heterozigosity (LOH) was described in 29% of the PETs. Since SDHD gene may depict a form of genomic imprinting in neuroendocrine (NE) tissue, the reported LOH may drive activation of the hypoxia pathway. Taking advantage from the immunohistochemical (IHC) method for genetic triage we may deduce the mutational status of SDH subunits (A, B, C and D) based on IHC SDHB expression. These subunits are striking candidates as they are mutated in other NE neoplasias.
Category: Basic
Presenting Author: Mr João Vinagre
Authors: Vinagre J, Preto J, Soares P, Lopes J M, ...
Keywords: PETs SDH LOH
#945 Interference of Nutrient/Oxygen Availability with mTOR Activation and Inhibition in Lung Carcinoids: A Tissue and Cellular Study
Introduction: MTOR is capable of coupling cellular nutrient sensing to metabolic homeostasis. However, little is known of the interactions between cancer‐specific metabolic pathways and profiles of responsiveness to mTOR inhibition in neuroendocrine tumors.
Conference: 11th Annual ENETS Conference (2014)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Prof Marco Volante
Authors: Rapa I, Giorcelli J, Votta A, Marino G, ...
#1557 Dual High Throughput Proteomic and Transcriptomic Screen for Predictive Biomarkers of Everolimus Sensitivity in Pancreatic NET
Introduction: mTOR inhibitor Everolimus is approved for the treatment of well-differentiated PNET. The heterogeneity of the response rate and the potential toxicity warrant predictive biomarkers.
Conference: 13th Annual ENETS conference (2016)
Category: Basic Science - mTOR and other pathways, signalling, receptors
Presenting Author: Dr Jerome Cros
Authors: Bucau M, Cros J, Raffenne J, Rebours V, ...
#1850 Influence of VEGF Splicing on Microvessel Density and Architecture in Pancreatic Neuroendocrine Tumours
Introduction: Hypoxia in human tumours is associated with a poor prognosis and is characterized by the stabilization of HIF1α, upregulation of VEGF, and a high microvessel density (MVD). Interestingly, although pancreatic neuroendocrine tumours (pNETS) showing hypoxia signalling also have a poor prognosis, they paradoxically display a low MVD. We hypothesized that this paradoxon might be explained by alternative splicing of VEGF.
Conference: 14th Annual ENETS conference (2017)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: MD Anja Maria Schmitt
Authors: Marinoni I, Naim S, Centeno I, Perren A, ...
Keywords: pNET, VEGF
#22 A Case Illustrative of Phenotypic Heterogeneity and Challenges in the Management of Paraganglioma
Introduction: Paragangliomas (PGLs) are extra-adrenal, usually benign, highly vascularized tumors that originate from neural-crest-derived chromaffin cells. These tumors are subdivided as either sympathetic or parasympathetic, depending on their location and catecholamine production. Sympathetic PGLs are situated along the abdominal sympathetic trunk and usually produce catecholamines, whereas parasympathetic PGLs are located in the head and neck, and these usually do not produce catecholamines. PGLs may present as sporadic or inherited tumor syndrome, including MEN 2, with RET germline mutations, von Hippel-Lindau (VHL) disease due to germline mutations in VHL gene, and pheochromocytoma-PGL syndrome. The latter is frequently a hereditary condition and is caused by germline mutations in the SDHB, SDHC, or SDHC genes. Patients with familial PGLs may present at a younger age, often as multifocal tumors, with an increased risk of recurrence and a higher frequency of malignancy in those with SDHB mutations. SDH mutations induce angiogenesis and tumorogenesis through the inhibition of hypoxia-inducible factors (HIF)-propyl hyroxylase. A younger age at onset, malignancy, and a positive family history are clinical parameters of high specificity, but low sensitivity for diagnosis. Genetic analysis for mutations in SDH genes for the patient and family members, and surveillance for the affected patient and family members, are necessary where there are no clear clinical or family indicators for the syndrome. We present a case of a large abdominal malignant PGL in a 20-year-old pt. that went on without clinical detection for at least three years.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Dr Mohammed Ahmed