Abstract library

3 results for "Circadian clock".
#2980 Metabolic Dysregulation and Circadian Clock in Cellular Models of Neuroendocrine Tumors
Introduction: The circadian clock genes encode transcription factors whose interaction with nuclear receptors allows the regulation of cellular metabolism.The invalidation of the genes of the clock core is associated with the development of many endocrine diseases including neuroendocrine cancer. Recently, the family of transcriptional coactivators PGC-1a has been identified as a key element in the integration of cellular metabolic state with the circadian clock. PRC, as a member of the PGC-1 family, was able to interact with several transcription factors, including the CLOCK factor. The specific induction of this PRC factor by the cell cycle, to modulate the energy function, the MAPkinase pathway and the expression of microRNAs, makes it a key factor in the metabolic adaptation of cancer cells.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Pr Frederique Savagner
#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
#374 Hyperammonemic Encephalopathy in Neuroendocrine Tumor Resolved Through Liver Embolization: A Case Report
Introduction: Gastroenteropancreatic neuroendocrine tumors are a rare cause of secondary hyperammonemic encephalopathy. Possible etiological mechanisms are global hepatic dysfunction secondary to tumor burden or microvascular portosystemic shunting in the liver metastases often present in GEP-NET.
Conference: 9th Annual ENETS Conference (2012)
Category: Clinical
Presenting Author: Timon Vandamme