about
The SRC-associated protein CUB Domain-Containing Protein-1 regulates adhesion and motilityNuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formationDepletion of a putatively druggable class of phosphatidylinositol kinases inhibits growth of p53-null tumors.PARK2 deletions occur frequently in sporadic colorectal cancer and accelerate adenoma development in Apc mutant mice.Inhibition of pyruvate kinase M2 by reactive oxygen species contributes to cellular antioxidant responsesPhosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling.Loss of INPP4B causes a DNA repair defect through loss of BRCA1, ATM and ATR and can be targeted with PARP inhibitor treatment.Metabolic stress controls mTORC1 lysosomal localization and dimerization by regulating the TTT-RUVBL1/2 complex.Identification of CDCP1 as a hypoxia-inducible factor 2α (HIF-2α) target gene that is associated with survival in clear cell renal cell carcinoma patientsIRS2 is a candidate driver oncogene on 13q34 in colorectal cancer.p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumoursDecreased function of survival motor neuron protein impairs endocytic pathways.DNA mismatch repair deficiency in sporadic colorectal cancer and Lynch syndrome.RAS signalling in the colorectum in health and disease.Proteomics profiling of interactome dynamics by colocalisation analysis (COLA).Synergism between K-rasVal12 and mutant Apc accelerates murine large intestinal tumourigenesis.Increased tumorigenesis associated with loss of the tumor suppressor gene Cadm1.Oncogenic KRAS Regulates Tumor Cell Signaling via Stromal Reciprocation.Oncogenic KRAS Regulates Tumor Cell Signaling via Stromal Reciprocation.K-ras exon 4A has a tumour suppressor effect on carcinogen-induced murine colonic adenoma formation.Mutated K-ras(Asp12) promotes tumourigenesis in Apc(Min) mice more in the large than the small intestines, with synergistic effects between K-ras and Wnt pathways.Mutant K-ras promotes carcinogen-induced murine colorectal tumourigenesis, but does not alter tumour chromosome stability.Prognostic relevance of DNA copy number changes in colorectal cancer.PARK2 Depletion Connects Energy and Oxidative Stress to PI3K/Akt Activation via PTEN S-Nitrosylation.Discovery of naturally occurring ESR1 mutations in breast cancer cell lines modelling endocrine resistance.Perioperative events influence cancer recurrence risk after surgery.PARK2 loss promotes cancer progression via redox-mediated inactivation of PTEN.DNA Damage, Repair, and Cancer Metabolism.Asparagine bioavailability governs metastasis in a model of breast cancer.Deconstructing the Metabolic Networks of Oncogenic Signaling Using Targeted Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS).Phosphoinositide 3-Kinase/Akt Signaling and Redox Metabolism in Cancer.Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation.Conditional expression of mutated K-ras accelerates intestinal tumorigenesis in Msh2-deficient miceWild-type K-ras has a tumour suppressor effect on carcinogen-induced murine colorectal adenoma formationNonsteroidal anti-inflammatory drugs and pain in cancer patients: a systematic review and reappraisal of the evidence
P50
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P50
description
researcher ORCID ID = 0000-0002-0529-8614
@en
wetenschapper
@nl
name
George Poulogiannis
@ast
George Poulogiannis
@en
George Poulogiannis
@es
George Poulogiannis
@nl
type
label
George Poulogiannis
@ast
George Poulogiannis
@en
George Poulogiannis
@es
George Poulogiannis
@nl
prefLabel
George Poulogiannis
@ast
George Poulogiannis
@en
George Poulogiannis
@es
George Poulogiannis
@nl
P108
P1153
16686659000
P21
P31
P496
0000-0002-0529-8614