ZMB Member Johann Matschke
ZMB Member
Johann Matschke
Next ZMB-Member
PD Dr. Johann Matschke
Institute of Cell Biology (Tumor Research)
University Hospital Essen
Virchowstr. 173
45122 Essen
- +49 201 723 4234
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- ZMB Research Program
Oncology
Research Overview
Our research focuses on the role of metabolic reprogramming in cancer cells for intrinsic, microenvironment-induced, and adaptive radioresistance and the identification of associated specific metabolic vulnerabilities of cancer cells suited to improve the cytotoxic efficacy of radiotherapy.
Therefore, we have established various specific in vitro methods for the analysis and evaluation of radiobiology endpoints, cell metabolite levels, real-time metabolic fluxes in normoxia and hypoxia (Seahorse Bioanalyser). We also perform time-resolved metabolome analyses with national and inter-national cooperation partners. Long-term goal is to develop effective strategies for a targeted cancer cell radiosensitization and to identify associated stratification markers.
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Selected Publications
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Balancing barriers: Family, career, and gender equality in radiation oncology and radiation research : An interdisciplinary prospective survey among the young workforceIn: Strahlentherapie und Onkologie: Journal of Radiation Oncology, Biology, Physics 2025 , in pressDOI (Open Access)
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Elevated NLRP3 Inflammasome Activation Is Associated with Motor Neuron Degeneration in ALSIn: Cells , Vol. 13 2024, Nr. 12, 995DOI (Open Access)
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German radiation oncology’s next generation : A web-based survey of young biologists, medical physicists, and physicians — from problems to solutionsIn: Strahlentherapie und Onkologie: Journal of Radiation Oncology, Biology, Physics , Vol. 200 2024, Nr. 12, pp. 1005 – 1024DOI (Open Access)
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Metabolic pathway-based subtypes associate glycan biosynthesis and treatment response in head and neck cancerIn: npj Precision Oncology , Vol. 8 2024, Nr. 1, 116DOI (Open Access)
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α-Ketoglutarate supplementation and NAD+ modulation enhance metabolic rewiring and radiosensitization in SLC25A1 inhibited cancer cellsIn: Cell Death Discovery , Vol. 10 2024, Nr. 1, 27DOI, Online Full Text (Open Access)
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A Sequential Targeting Strategy Interrupts AKT-Driven Subclone-Mediated Progression in GlioblastomaIn: Clinical Cancer Research , Vol. 29 2023, Nr. 2, pp. 488 – 500DOI (Open Access)
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Cigarette smoke causes a bioenergetic crisis in RPE cells involving the downregulation of HIF-1α under normoxiaIn: Cell Death Discovery , Vol. 9 2023, Nr. 1, 398DOI, Online Full Text (Open Access)
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The second PI(3,5)P₂binding site in the S0 helix of KCNQ1 stabilizes PIP₂-at the primary PI1 site with potential consequences on intermediate-to-open state transitionIn: Biological Chemistry , Vol. 404 2023, Nr. 4, pp. 241 – 254
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Accumulation of oncometabolite D-2-Hydroxyglutarate by SLC25A1 inhibition: A metabolic strategy for induction of HR-ness and radiosensitivityIn: Cell Death and Disease , Vol. 13 2022, Nr. 7, 641DOI, Online Full Text (Open Access)
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Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reactionIn: Cell Death and Disease , Vol. 13 2022, Nr. 7, 662DOI, Online Full Text (Open Access)
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ROS scavengers decrease γH2ax spots in motor neuronal nuclei of ALS model mice in vitroIn: Frontiers in Cellular Neuroscience , Vol. 16 2022, 963169DOI (Open Access)
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Targeting AKT-Dependent Regulation of Antioxidant Defense Sensitizes AKT-E17K Expressing Cancer Cells to Ionizing RadiationIn: Frontiers in Oncology , Vol. 12 2022, 920017DOI, Online Full Text (Open Access)
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Adaptation to chronic-cycling hypoxia renders cancer cells resistant to mth1-inhibitor treatment which can be counteracted by glutathione depletionIn: Cells , Vol. 10 2021, Nr. 11, 3040DOI, Online Full Text (Open Access)
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Increased ROS-Dependent Fission of Mitochondria Causes Abnormal Morphology of the Cell Powerhouses in a Murine Model of Amyotrophic Lateral SclerosisIn: Oxidative Medicine and Cellular Longevity , Vol. 2021 2021, 6924251DOI (Open Access)
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Metabolic reprograming of antioxidant defense : A precision medicine perspective for radiotherapy of lung cancer?In: Biochemical Society Transactions , Vol. 49 2021, Nr. 3, pp. 1265 – 1277
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Metabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdownIn: iScience , Vol. 24 2021, Nr. 11, 103366DOI (Open Access)
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A new twist in protein kinase b/akt signaling : Role of altered cancer cell metabolism in akt-mediated therapy resistanceIn: International Journal of Molecular Sciences (IJMS) , Vol. 21 2020, Nr. 22, pp. 8563DOI, Online Full Text (Open Access)
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Oncometabolites and the response to radiotherapyIn: Radiation Oncology , Vol. 15 2020, pp. 197DOI, Online Full Text (Open Access)
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Proton Irradiation Increases the Necessity for Homologous Recombination Repair Along with the Indispensability of Non-Homologous End JoiningIn: Cells , Vol. 9 2020, Nr. 4, pp. 889DOI, Online Full Text (Open Access)
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Oxidative stress: the lowest common denominator of multiple diseasesIn: Neural Regeneration Research , Vol. 14 2019, Nr. 2, pp. 238 – 241DOI (Open Access)
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Sequence-dependent cross-resistance of combined radiotherapy plus BRAFV⁶⁰⁰E inhibition in melanomaIn: European Journal of Cancer (EJC) , Vol. 109 2019, pp. 137 – 153
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Targeting SLC25A10 alleviates improved antioxidant capacity and associated radioresistance of cancer cells induced by chronic-cycling hypoxiaIn: Cancer Letters , Vol. 439 2018, pp. 24 – 38
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The Mitochondrial Citrate Carrier (SLC25A1) Sustains Redox Homeostasis and Mitochondrial Metabolism Supporting Radioresistance of Cancer Cells With Tolerance to Cycling Severe HypoxiaIn: Frontiers in Oncology , Vol. 8 2018, pp. 170DOI, Online Full Text (Open Access)
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Role of SGK1 for fatty acid uptake, cell survival and radioresistance of NCI-H460 lung cancer cells exposed to acute or chronic cycling severe hypoxiaIn: Radiation Oncology , Vol. 11 2016, Nr. 1, pp. 75 – 87DOI (Open Access)
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Targeted Inhibition of Glutamine-Dependent Glutathione Metabolism Overcomes Death Resistance Induced by Chronic Cycling HypoxiaIn: Antioxidants and Redox Signaling , Vol. 25 2016, Nr. 2, pp. 89 – 107
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The Natural Plant Product Rottlerin Activates Kv7.1/KCNE1 ChannelsIn: Cellular Physiology and Biochemistry , Vol. 40 2016, Nr. 6, pp. 1549 – 1558DOI (Open Access)
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Chronic intermittent hypoxia triggers adaptive changes that promote protection against cell deathIn: European Journal of Cancer (EJC) , Vol. 49 2013, Nr. Suppl. 2, pp. 101