Cornelis J.F. Van Noorden

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BACKGROUND High-dose radiotherapy is standard treatment for patients with brain cancer. However, in preclinical research external beam radiotherapy is limited to heterotopic murine models- high-dose radiotherapy to the murine head is fatal due to radiation toxicity. Therefore, we developed a stereotactic brachytherapy mouse model for high-dose focal(More)
Ocular diseases dominated by neovascularization, such as age-related macular degeneration (AMD), retinal vein occlusions, and diabetic retinopathy (DR), often culminate in severe visual loss and ultimately blindness. In most of these conditions, ischemic retinal areas produce abnormal amounts of angiogenic growth factors that induce excessive angiogenesis,(More)
BACKGROUND Point mutations in genes encoding NADP+-dependent isocitrate dehydrogenases (especially IDH1) are common in lower grade diffuse gliomas and secondary glioblastomas and occur early during tumor development. The contribution of these mutations to gliomagenesis is not completely understood and research is hampered by the lack of relevant tumor(More)
OBJECTIVE Increased levels of vascular endothelial growth factor (VEGF) in human plasma samples have suggested that circulating VEGF is a cause of endothelial dysfunction in diabetes mellitus. However, artificial release of VEGF from platelets as a source of VEGF in plasma samples, as also occurs in serum samples, has not been ruled out in these studies. (More)
Glioblastoma multiforme (GBM) is the most common and most aggressive malignant primary brain tumor in humans. Current GBM treatment includes surgery, radiation therapy, and chemotherapy, sometimes supplemented with novel therapies. Despite recent advances, survival of GBM patients remains poor. Major challenges in GBM treatment are drug delivery across the(More)
Glutamate dehydrogenase (GDH) catalyses the reversible conversion of glutamate into α-ketoglutarate with the concomitant reduction of NAD(P)(+) to NAD(P)H or vice versa. GDH activity is subject to complex allosteric regulation including substrate inhibition. To determine GDH kinetics in situ, we assessed the effects of various glutamate concentrations in(More)
Glioblastoma is a highly malignant brain tumor for which no cure is available. To identify new therapeutic targets, we performed a mutation analysis of kinase genes in glioblastoma. Database mining and a literature search identified 76 kinases that have been found to be mutated at least twice in multiple cancer types before. Among those we selected 34(More)
Phosphate-activated glutaminase (PAG) converts glutamine to glutamate as part of the glutaminolysis pathway in mitochondria. Two genes, GLS1 and GLS2, which encode for kidney-type PAG and liver-type PAG, respectively, differ in their tissue-specific activities and kinetics. Tissue-specific PAG activity and its kinetics were determined by metabolic mapping(More)
fNTRODUCTION Quantitative enzyme histochemistry allows for the demonstration of enzyme activities at the cellular level. It is a light microscopical techmque, mostly applied to unfixed tissue sections so as to determine the amount and localization of coloured reaction products generated by enzyme activities. Enzyme histochemistry has the advantage of high(More)
The metabolic consequences of the NADP +-dependent isocitrate dehydrogenase (IDH) 1 mutation was studied quantitatively in glioblastoma, the most aggressive form of brain tumor. The mutation is found in 70-80% of secondary glioblastoma. Metabolic rewiring of cells due to the mutation causes gliomagenesis by the production of 2-hydroxyglutarate. On the other(More)