4 results for "knock-out".
Introduction: An important limiting factor influencing treatment efficacy of neuroendocrine tumors (NETs) with somatostatin analogs (SSA) is the availability of somatostatin receptors (SSTR) on NETs. While downregulation or altered pattern of SSTR expression are important considerations, receptor internalization/desensitization by β-arrestins may be a crucial contributing factor. Interestingly, our previous study showed a preferential higher expression of β-arrestin 1 (ARRB1), in gastroenteropancreatic NETS (GEP-NETs) compared to pituitary adenomas.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Basic Science - Signaling pathways, receptors, biomarkers
Presenting Author: Dr Anand Iyer
Introduction: The current study explores novel targeted therapies for malignant pheochromocytomas (PCCs) and paragangliomas, utilizing a more benign (MPC) and a more malignant (MTT) PCC cell line. We have previously shown that the dual PI3K/mTORC1 inhibitor NVP-BEZ235 significantly reduced MPC and MTT cell viability, but increased ERK signalling.
Conference: 9th Annual ENETS Conference (2012)
Presenting Author: Dr Svenja Noelting
Introduction: There are four main types of thyroid cancer, papillary (PTC), follicular (FTC), medullary (MTC), and anaplastic. In both PTC and MTC, genomic rearrangements and point mutations in the proto-oncogene RET are common. RET encodes a receptor tyrosine kinase that is negatively regulated by leucine-rich repeats and immunoglobulin-like domains-1 (LRIG1). LRIG1 gene status and mRNA and protein expression correlate with patient survival in different types of cancer.
Conference: 14th Annual ENETS conference 2017 (2017)
Presenting Author: Associate profes David Lindquist
Introduction: Cancer driver mutations affecting the histone H3.3 chromatin remodellers ATRX and DAXX were recently discovered in 43% of sporadic pancreatic neuroendocrine tumours (PNET). Progressive age-dependent replacement of canonical H3.1/2 with H3.3 is crucial for maintaining genome integrity through expression of repressive markers at heterochromatic sites, where loading is mediated by ATRX and DAXX. Loss of H3.3 chaperones in PNET is associated with activation of ALT, a telomere maintenance mechanism, eventually leading to chromosome instability. It has been suggested that ATRX/DAXX expression is necessary for repressing ALT, but mechanistic details of this interaction are not fully understood.
Conference: 15th Annual ENETS conference 2018 (2018)
Category: Basic Science - In vitro models, tumor growth, CTCs
Presenting Author: PhD Student Teresa Sposito