Andrea Kutritz
A5074183297- Cancer, Hypoxia, and Metabolism
- Metabolism, Diabetes, and Cancer
- Cancer, Lipids, and Metabolism
- Selenium in Biological Systems
- Lung Cancer Treatments and Mutations
- Cancer Treatment and Pharmacology
- Redox biology and oxidative stress
- Neuroblastoma Research and Treatments
- Neurofibromatosis and Schwannoma Cases
- Pain Mechanisms and Treatments
- Sarcoma Diagnosis and Treatment
- Glioma Diagnosis and Treatment
- Protein Degradation and Inhibitors
- Chromatin Remodeling and Cancer
- Nerve injury and regeneration
- Hereditary Neurological Disorders
- Nanoplatforms for cancer theranostics
- Neuroscience and Neuropharmacology Research
- Ion Channels and Receptors
- Hedgehog Signaling Pathway Studies
- S100 Proteins and Annexins
- Vascular Tumors and Angiosarcomas
- Ion channel regulation and function
- Musculoskeletal synovial abnormalities and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
Essen University Hospital
2020-2025
Deutschen Konsortium für Translationale Krebsforschung
2025
University of Duisburg-Essen
2011-2020
Abstract In patients with non–small cell lung cancer (NSCLC), the relationship between tumor metabolism and clinical outcomes is unknown. Here, 13C-labeled nutrients were intraoperatively infused into more than 90 surgically resectable pulmonary lesions, metabolic properties of resected tumors correlated survival. NSCLCs 13C-glucose, high 13C enrichment in tricarboxylic acid (TCA) cycle intermediates conferred a HR 3.8 for early death, typically metastasis. To test whether these features...
Cisplatin and oxaliplatin are treatment options for a variety of cancer types. While highly efficient in killing cells, both chemotherapeutics cause severe side effects, e.g., peripheral neuropathies. Using cell viability assay, mitochondrial stress live-cell imaging, the effects cis- or on function, reactive oxygen species (ROS) production, cytosolic calcium concentration transient receptor potential ankyrin 1 (TRPA1)- vanilloid (TRPV1)-positive dorsal root ganglion (DRG) neurons adult...
<p>Supplementary Figure S4 depicts characterization of SelenoO deficient cell lines</p>
<p>Supplementary Figure S7 shows mass spectra of SdhA and Aco2</p>
<p>Supplementary Figure S2 correlates SelenoO expression with survival and metastasis</p>
<p>Supplemental data file contains Table S1, S2 and Figures S1-S7</p>
<p>Supplementary Figure S3 depicts expression of SelenoO in cell lines used this study</p>
<p>Supplementary Figure S6 depicts markers of subcellular fractionation used to isolate crude mitochondria.</p>
<p>Supplementary Figure S5 shows redox metabolite levels in wildtype and SelenoO deficient cell lines.</p>
<p>Data table of AMPylated substrates identified by mass spectrometry analysis.</p>
<div>Abstract<p>Evolutionarily conserved selenoprotein O (SELENOO) catalyzes a posttranslational protein modification known as AMPylation that is essential for the oxidative stress response in bacteria and yeast. Given experienced blood limits survival of metastasizing melanoma cells, SELENOO might be able to affect metastatic potential. However, further work needed elucidate substrates functional relevance mammalian homolog SELENOO. In this study, we revealed promotes cancer...
<p>Supplementary Figure S1 shows expressions of SelenoO in cancer subtypes</p>
<div>Abstract<p>In patients with non–small cell lung cancer (NSCLC), the relationship between tumor metabolism and clinical outcomes is unknown. Here, <sup>13</sup>C-labeled nutrients were intraoperatively infused into more than 90 surgically resectable pulmonary lesions, metabolic properties of resected tumors correlated survival. In NSCLCs <sup>13</sup>C-glucose, high <sup>13</sup>C enrichment in tricarboxylic acid (TCA) cycle intermediates...
<p>(Related to Figure 1). TCA cycle labeling and metabolite abundance in tumors lungs from NSCLC patents.</p>
<p>(Related to Figure 4). Development of patient-derived xenografts from malignant tumors in the lung.</p>
<p>(Related to Figure 3). TCA cycle metabolite abundance does not correlate with overall survival.</p>
<p>Increased <sup>13</sup>C enrichment in the TCA cycle predicts reduced survival. <b>A,</b><sup>13</sup>C adjacent lung and tumors with high or low labeling. Fractional enrichments of glycolytic (M+3) (M+2) metabolites are normalized to glucose (M+6) within tissue. <b>B</b> <b>C,</b> Overall (<b>B</b>) recurrence-free (<b>C</b>) survival patients whose have The groups include above below median for...
<p>Inhibition of complex I with IACS-010759 limits metastasis in NSCLC PDXs. <b>A</b> and <b>B,</b> Tumor-bearing mice were treated daily DMSO or (5 mg/kg) by oral gavage for 3–4 weeks then infused [U-<sup>13</sup>C]glucose 3 hours. Overall TCA cycle enrichment was calculated as the sum isotopologues citrate, malate, glutamate compared between DMSO- IACS-010759–treated groups. <b>C</b> <b>D,</b> Subcutaneous tumor volume (L ×...
<p>PDXs derived from primary NSCLC retain histological, molecular, and metabolic characteristics. <b>A</b> <b>B,</b> Summary of histological molecular characterization donor tumors (<b>A</b>) PDX models (<b>B</b>). <b>C,</b> H&E staining PDXs. <b>D,</b> Engraftment success NSCLCs lung metastases considering the phenotype patient’s tumor. “High” “low” TCA cycle enrichment was defined in <a href="#fig3"...
<p>PDXs generated from primary NSCLCs spontaneously metastasize in NSG mice. <b>A,</b> Flow cytometry analysis of lung tissue a mouse engrafted with mx73. Cells were stained lineage markers (CD45, CD31, and TER119) HLA. <b>B,</b> Bioluminescence lungs bearing metastases <b>C,</b> IHC staining for Ki67-positive cells metastasis mx148. <b>D,</b> Percentage HLA-ABC–expressing detected the mice NSCLC PDXs. Each dot represents one mouse. Data...