Publications by authors named "M W Ronellenfitsch"
Background: Diffuse hemispheric glioma, histone 3 (H3) G34-mutant, has been newly defined in the 2021 WHO classification of central nervous system tumors. Here we sought to define the prognostic roles of clinical, neuroimaging, pathological, and molecular features of these tumors.
Methods: We retrospectively assembled a cohort of 114 patients (median age 22 years) with diffuse hemispheric glioma, H3 G34-mutant, CNS WHO grade 4 and profiled the imaging, histological and molecular landscape of their tumors.
Article Synopsis
- The study investigates the use of cell-free DNA (cfDNA) from cerebrospinal fluid (CSF) as a less invasive alternative to brain biopsies for diagnosing brain tumors and addressing tumor heterogeneity.
- A total of 33 CSF samples were collected from 30 patients, and shallow whole-genome sequencing was performed, revealing significant somatic copy number aberrations (SCNAs) in brain tumor patients' cfDNA.
- The findings suggest that cfDNA analysis can effectively identify relevant genomic alterations, offering insights into tumor evolution and heterogeneity, thus enhancing diagnostic accuracy for CNS cancers.
Glioblastoma, the most frequent primary malignant brain tumour in adults, is characterised by profound yet dynamic hypoxia and nutrient depletion. To sustain survival and proliferation, tumour cells are compelled to acquire metabolic plasticity with the induction of adaptive metabolic programs. Here, we interrogated the pathways necessary to enable processing of nutrients other than glucose.
View Article and Find Full Text PDFPurpose: Reprogramming of amino acid metabolism is relevant for initiating and fueling tumor formation and growth. Therefore, there has been growing interest in anticancer therapies targeting amino acid metabolism. While developing personalized therapeutic approaches to glioma, in vivo proton magnetic resonance spectroscopy (MRS) is a valuable tool for non-invasive monitoring of tumor metabolism.
View Article and Find Full Text PDFIn glioblastoma (GB) cells oxidative stress is induced by both, conditions of the tumor microenvironment as well as by therapeutic interventions. Upregulation of superoxide dismutase 1 (SOD1), a key enzyme for oxidative defense and downstream target of mammalian target of rapamycin complex 1 (mTORC1) is a candidate mechanism to sustain survival and proliferation of tumor cells. SOD1 was inhibited by shRNA mediated gene suppression, CRISPR/Cas9 knockout and pharmacological inhibition in human (primary) GB cells.
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