Results 61 to 70 of about 426,683 (300)
CEACAM1 participation in breast cancer progression
Molecular Oncology, EarlyView.In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin +3 more
wiley +1 more source
Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
Molecular Oncology, EarlyView.Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas +16 more
wiley +1 more source
The Egyptian Journal of Critical Care Medicine, 2016 AbstractThe indication and usage for Extracorporeal Life Support (ECLS) has increased significantly over the last 10years, and more and more hospitals are now offering this service. Despite this trend, ECLS is a mature “daily business” in only a few centers.In this context, the importance of simulation in the field of ECLS must be strongly emphasized ...
openaire +2 more sources
Molecular Oncology, EarlyView.This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi +6 more
wiley +1 more source
Molecular Oncology, EarlyView.In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico +5 more
wiley +1 more source
Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation
Molecular Oncology, EarlyView.How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim +11 more
wiley +1 more source
, 2005 The ECL cells in the oxyntic mucosa secrete histamine in response to gastrin, stimulating parietal cells to produce acid. Do they also operate under nervous control?
Ericsson, Peter +9 more
core +1 more source
Reprogramming tumor cells with LCOR mRNA nanotherapy to enhance immunotherapy
Molecular Oncology, EarlyView.LCOR (Ligand‐dependent corepressor) mRNA encapsulated in polymeric nanoparticles restores LCOR activity in tumor cells, constraining aggressive tumor cell states and increasing tumor immunogenicity. This reprogramming makes tumor cells more vulnerable to T‐cell attack and enhances their response to immune‐checkpoint immunotherapy.
Gabriel Serra‐Mir +9 more
wiley +1 more source