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1. Full Text Rescue of 2-deoxyglucose side effects by ketogenic diet
by Voss, Martin and Lorenz, Nadja I and Luger, Anna-Luisa and Steinbach, Joachim P and Rieger, Johannes and Ronellenfitsch, Michael W
International Journal of Molecular Sciences, ISSN 1661-6596, 08/2018, Volume 19, Issue 8, p. 2462
Cancer metabolism is characterized by extensive glucose consumption through aerobic glycolysis. No effective therapy exploiting this cancer trait has emerged... 
Glycolysis | Isocaloric ketogenic diet | Metabolic cancer therapy | 2-deoxyglucose (2-DG) | Warburg effect | MAMMALIAN TARGET | GLIOMA-CELLS | isocaloric ketogenic diet | BEVACIZUMAB | BIOCHEMISTRY & MOLECULAR BIOLOGY | glycolysis | 2-DEOXY-D-GLUCOSE | HYPOXIA | CHEMISTRY, MULTIDISCIPLINARY | DOSE-ESCALATION | INHIBITION | THERAPY | METABOLISM | metabolic cancer therapy | CANCER RADIOTHERAPY | Neoplasms - metabolism | Diet, Ketogenic - methods | Ketone Bodies - metabolism | Ketosis - etiology | Glycolysis - drug effects | Antimetabolites - administration & dosage | Antimetabolites - adverse effects | Animals | Deoxyglucose - adverse effects | Mice, Nude | Deoxyglucose - administration & dosage | Glucose - metabolism | Female | Ketosis - metabolism | Blood Glucose - metabolism | Carbohydrates | Therapy | Ketogenesis | Ketone bodies | Glucose | Metabolism | Deoxyglucose | Proteins | Side effects | Diet | Mice | Cancer | Phosphorylation | Alternative energy | Brain cancer | Kinases | Cancer therapies | Hyperglycemia | Drug dosages | Radiation therapy | Hypoglycemia | Chemotherapy | Hypoxia | Apoptosis | Tumors
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2. Full Text Bevacizumab for patients with recurrent multifocal glioblastomas
by Burger, Michael C and Breuer, Stella and Cieplik, Hans C and Harter, Patrick N and Franz, Kea and Bähr, Oliver and Steinbach, Joachim P
International Journal of Molecular Sciences, ISSN 1661-6596, 11/2017, Volume 18, Issue 11, p. 2469
In patients with glioblastoma, antiangiogenic therapy with bevacizumab (BEV) has been shown to improve progression-free survival (PFS), but not overall... 
Multifocal | Anti-angiogenic therapy | Infiltration | Glioblastoma | Invasive growth | Bevacizumab | SURVIVAL | anti-angiogenic therapy | NEWLY-DIAGNOSED GLIOBLASTOMA | LOMUSTINE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CHEMISTRY, MULTIDISCIPLINARY | infiltration | TEMOZOLOMIDE | invasive growth | MALIGNANT GLIOMA | TRIAL | INVASION | glioblastoma | THERAPY | multifocal | bevacizumab | RADIOTHERAPY | PROGRESSION | Therapy | Nuclear magnetic resonance--NMR | Brain cancer | Patients | Survival | Cancer therapies | Irinotecan | Magnetic resonance imaging | Antiangiogenics | Medical prognosis | Lesions
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3. Full Text Gene suppression of transketolase-like protein 1 (TKTl1) sensitizes glioma cells to hypoxia and ionizing radiation
by Heller, Sonja and Maurer, Gabriele D and Wanka, Christina and Hofmann, Ute and Luger, Anna-Luisa and Bruns, Ines and Steinbach, Joachim P and Rieger, Johannes
International Journal of Molecular Sciences, ISSN 1661-6596, 08/2018, Volume 19, Issue 8, p. 2168
In several tumor entities, transketolase-like protein 1 (TKTL1) has been suggested to promote the nonoxidative part of the pentose phosphate pathway (PPP) and... 
Pentose phosphate pathway | Hypoxia | Transketolase-like protein 1 | Glioma | Metabolism | Radiation | TARGET | hypoxia | ACTIVATION | PENTOSE-PHOSPHATE PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | transketolase-like protein 1 | CHEMISTRY, MULTIDISCIPLINARY | pentose phosphate pathway | GLYCOLYSIS | INDUCIBLE FACTORS | GLIOBLASTOMA | PROTECTS GLIOMA | radiation | glioma | metabolism | RECURRENCE | EXPRESSION | PROGRESSION | Hypoxia-inducible factors | Pentose phosphate | Deprivation | Oxygen | Phenotypes | Reactive oxygen species | Tumor cells | Transketolase | Radioresistance | Survival | Impact analysis | Proteins | Ionizing radiation | Cell death | Antiangiogenics | Glioma cells | Pentose | Irradiation | Tumors
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4. Full Text Intracellular pH measured by 31P‐MR‐spectroscopy might predict site of progression in recurrent glioblastoma under antiangiogenic therapy
by Wenger, Katharina J and Hattingen, Elke and Franz, Kea and Steinbach, Joachim P and Bähr, Oliver and Pilatus, Ulrich
Journal of Magnetic Resonance Imaging, ISSN 1053-1807, 10/2017, Volume 46, Issue 4, pp. 1200 - 1208
Purpose In solid tumors, changes in the expression/activity of plasma membrane ion transporters facilitate proton efflux and enable tumor cells to maintain a... 
pHi | bevacizumab | 31P‐MR‐spectroscopy | glioblastoma | tumor progression | pH | P-MR-spectroscopy | Antimitotic agents | Brain tumors | Spectrum analysis | Development and progression | Hydrogen-ion concentration | Antineoplastic agents | Glioblastoma multiforme | Neuroimaging | Brain | Efflux | Spectroscopy | Nuclear magnetic resonance--NMR | Tumor cells | Glioblastoma | Medical services | Oncology | pH effects | Patients | Bevacizumab | Magnetic resonance imaging | Hydrogen ions | Antiangiogenics | Solid tumors | Intracellular | Tumors
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5. Full Text Knockdown of the TP53-induced glycolysis and apoptosis regulator (TIGAR) sensitizes glioma cells to hypoxia, irradiation and temozolomide
by Maurer, Gabriele D and Heller, Sonja and Wanka, Christina and Rieger, Johannes and Steinbach, Joachim P
International Journal of Molecular Sciences, ISSN 1661-6596, 03/2019, Volume 20, Issue 5, p. 1061
The TP53-induced glycolysis and apoptosis regulator (TIGAR) has been shown to decrease glycolysis, to activate the pentose phosphate pathway, and to provide... 
Reactive oxygen species | Glioma | TP53-induced glycolysis and apoptosis regulator | Hypoxia-inducible factor | Irradiation | Hypoxia | Temozolomide | temozolomide | hypoxia | PROGNOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | hypoxia-inducible factor | IDENTIFICATION | CHEMISTRY, MULTIDISCIPLINARY | irradiation | P53 | PROTECTS | HIF-1 | GLIOBLASTOMA | RADIOSENSITIZATION | MICROENVIRONMENT | reactive oxygen species | glioma | TUMOR-SUPPRESSOR | PROGRESSION
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6. Full Text Delay in diagnosing patients with right-sided glioblastoma induced by hemispheric-specific clinical presentation
by Baumann, Claudia and Tichy, Julia and Schaefer, Jan Hendrik and Steinbach, Joachim P and Mittelbronn, Michel and Wagner, Marlies and Foerch, Christian
Journal of Neuro-Oncology, ISSN 0167-594X, 11/2019
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7. Full Text Loss of cell-matrix contact increases hypoxia-inducible factor-dependent transcriptional activity in glioma cells
by Maurer, Gabriele D and Brucker, Daniel P and Steinbach, Joachim P
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 07/2019, Volume 515, Issue 1, pp. 77 - 84
In a variety of malignomas, the acquisition of a mesenchymal phenotype has been linked with anchorage-independent growth and invasiveness. To some extent,... 
Hypoxia-inducible factor | Epithelial-mesenchymal transition | Anoikis | Reactive oxygen species | Glioblastoma | PATHWAYS | SUBTYPES | BIOCHEMISTRY & MOLECULAR BIOLOGY | MECHANISMS | MESENCHYMAL TRANSITION | BETA-CATENIN | BIOPHYSICS | ADAPTATION | GROWTH-FACTOR | EXPRESSION | Genetic aspects | Genetic transcription | Gliomas | Cell death | Stem cells
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8. Full Text Contrast enhancing spots as a new pattern of late onset pseudoprogression in glioma patients
by Voss, Martin and Franz, Kea and Steinbach, Joachim P and Fokas, Emmanouil and Forster, Marie-Thérèse and Filipski, Katharina and Hattingen, Elke and Wagner, Marlies and Breuer, Stella
Journal of Neuro-Oncology, ISSN 0167-594X, 3/2019, Volume 142, Issue 1, pp. 161 - 169
Magnet resonance imaging (MRI) of gliomas is assessed by Response Assessment in Neuro-Oncology Criteria (RANO), which define new contrast-enhancing lesions as... 
Brain tumor | Neurology | Medicine & Public Health | Glioma | Radionecrosis | Isocitrat dehydrogenase (IDH) | Oncology | Pseudoprogression | IDH1 | MGMT PROMOTER METHYLATION | CLINICAL NEUROLOGY | ADJUVANT TEMOZOLOMIDE | MALFORMATIONS | ONCOLOGY | PREDICT | CONCOMITANT | RADIATION NECROSIS | GRADE | RADIOTHERAPY | BRAIN | Magnetic Resonance Imaging | Glioma - diagnostic imaging | Image Processing, Computer-Assisted | Brain Neoplasms - diagnostic imaging | Humans | Middle Aged | Adult | Female | Male | Retrospective Studies | Disease Progression | Stroke (Disease) | Development and progression | Gliomas | Brain tumors | Radiation | Stroke | Vascular diseases | Magnetic resonance imaging | Ischemia | Glioblastoma | Radiation therapy | Diagnosis
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9. Full Text 18F-FET PET imaging in differentiating glioma progression from treatment-related changes – a single-center experience
by Maurer, Gabriele D and Brucker, Daniel P and Stoffels, Gabriele and Filipski, Katharina and Filss, Christian P and Mottaghy, Felix M and Galldiks, Norbert and Steinbach, Joachim P and Hattingen, Elke and Langen, Karl-Josef
Journal of Nuclear Medicine, ISSN 0161-5505, 09/2019, p. jnumed.119.234757
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10. Full Text EGFR and mTOR as therapeutic targets in glioblastoma
by Ronellenfitsch, Michael W and Luger, Anna-Luisa and Steinbach, Joachim P
Oncotarget, ISSN 1949-2553, 07/2019, Volume 10, Issue 46, p. 4721
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11. Full Text Disruption of peroxisome proliferator–activated receptor coactivator (PGC)-1 reverts key features of the neoplastic phenotype of glioma cells
by Bruns, Ines and Sauer, Benedikt and Burger, Michael C and Eriksson, Jule and Hofmann, Ute and Braun, Yannick and Harter, Patrick N and Luger, Anna-Luisa and Ronellenfitsch, Michael W and Steinbach, Joachim P and Rieger, Johannes
Journal of Biological Chemistry, ISSN 0021-9258, 2019, Volume 294, Issue 9, pp. 3037 - 3050
The peroxisome proliferator-activated receptor coactivator (PGC)-1 is a master regulator of mitochondrial biogenesis and controls metabolism by coordinating... 
MAMMALIAN TARGET | CANCER-CELLS | hypoxia | MITOCHONDRIAL BIOGENESIS | VEGF | BIOCHEMISTRY & MOLECULAR BIOLOGY | reactive oxygen species (ROS) | GLUCOSE TRANSPORTERS | glioblastoma | PROTECTS GLIOMA | METABOLISM | peroxisome proliferator-activated receptor coactivator 1-(PGC-1) (PPARGC1A) | RESPIRATION | transcription coactivator | EXPRESSION | tumor metabolism | GAMMA COACTIVATOR-1
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12. Full Text Disruption of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α reverts key features of the neoplastic phenotype of glioma cells
by Bruns, Ines and Sauer, Benedikt and Burger, Michael C and Eriksson, Jule and Hofmann, Ute and Braun, Yannick and Harter, Patrick N and Luger, Anna-Luisa and Ronellenfitsch, Michael W and Steinbach, Joachim P and Rieger, Johannes
The Journal of biological chemistry, ISSN 0021-9258, 03/2019, Volume 294, Issue 9, pp. 3037 - 3050
The peroxisome proliferator-activated receptor γ coactivator (PGC)-1α is a master regulator of mitochondrial biogenesis and controls metabolism by coordinating... 
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13. Full Text Doxycycline impairs mitochondrial function and protects human glioma cells from hypoxia-induced cell death: Implications of using tet-inducible systems
by Luger, Anna-Luisa and Sauer, Benedikt and Lorenz, Nadja I and Engel, Anna L and Braun, Yannick and Voss, Martin and Harter, Patrick N and Steinbach, Joachim P and Ronellenfitsch, Michael W
International Journal of Molecular Sciences, ISSN 1661-6596, 05/2018, Volume 19, Issue 5, p. 1504
Inducible gene expression is an important tool in molecular biology research to study protein function. Most frequently, the antibiotic doxycycline is used for... 
Mitochondria | Tumor metabolism | Doxycycline | Glioblastoma | Hypoxia-induced cell death | Tet-inducible system | Inducible gene expression | Tetracycline | MAMMALIAN TARGET | inducible gene expression | STEM-CELLS | ACTIVATION | mitochondria | BIOCHEMISTRY & MOLECULAR BIOLOGY | doxycycline | CHEMISTRY, MULTIDISCIPLINARY | hypoxia-induced cell death | MALIGNANT GLIOMA | glioblastoma | INHIBITION | RIBOSOMES | tetracycline | BINDING | EXPRESSION | tumor metabolism
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14. Full Text Fitting algorithms and baseline correction influence the results of non-invasive in vivo quantitation of 2-hydroxyglutarate with 1 H-MRS
by Wenger, Katharina J and Hattingen, Elke and Harter, Patrick N and Richter, Christian and Franz, Kea and Steinbach, Joachim P and Bähr, Oliver and Pilatus, Ulrich
NMR in Biomedicine, ISSN 0952-3480, 01/2019, Volume 32, Issue 1, p. e4027
H-MRS enables non-invasive detection of 2-hydroxyglutarate (2-HG), an oncometabolite accumulating in gliomas carrying mutations in the isocitrate dehydrogenase... 
glioma | 2-hydroxyglutarate | post-processing analysis | H-MRS | mutations in the IDH genes
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15. Full Text Akt and mTORC1 signaling as predictive biomarkers for the EGFR antibody nimotuzumab in glioblastoma
by Ronellenfitsch, Michael W and Zeiner, Pia S and Mittelbronn, Michel and Urban, Hans and Pietsch, Torsten and Reuter, Dirk and Senft, Christian and Steinbach, Joachim P and Westphal, Manfred and Harter, Patrick N
Acta neuropathologica communications, ISSN 2051-5960, 08/2018, Volume 6, Issue 1, pp. 81 - 13
Glioblastoma (GB) is the most frequent primary brain tumor in adults with a dismal prognosis despite aggressive treatment including surgical resection,... 
Biomarker | Targeted therapy | Epidermal growth factor receptor | Nimotuzumab | Glioblastoma | Mammalian target of rapamycin | MAMMALIAN TARGET | RAPAMYCIN | MALIGNANT GLIOMA-CELLS | ACTIVATION | PHASE-II | HYPOXIA | NEUROSCIENCES | ADJUVANT TEMOZOLOMIDE | GROWTH-FACTOR RECEPTOR | GRADE GLIOMAS | RADIOTHERAPY | Humans | Glioblastoma - diet therapy | Male | Quinazolines | DNA-Binding Proteins - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Time Factors | Antibodies, Monoclonal, Humanized - pharmacology | DNA Repair Enzymes - metabolism | Female | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Tumor Suppressor Proteins - metabolism | Antibodies, Monoclonal, Humanized - therapeutic use | DNA Modification Methylases - metabolism | Necrosis - metabolism | Treatment Outcome | Brain Neoplasms - drug therapy | Mechanistic Target of Rapamycin Complex 1 - metabolism | Signal Transduction - drug effects | Ribosomal Protein S6 - metabolism | ErbB Receptors - immunology | Necrosis - etiology | Adaptor Proteins, Signal Transducing - metabolism | Cohort Studies | Viral antibodies | Chemotherapy | Epidermal growth factor | Prognosis | Analysis | Brain tumors | Antibodies | Biological markers | Health aspects | Glioblastoma multiforme | Cancer | Phosphorylation | Brain cancer | Clinical trials | Vaccines | Radiation therapy | Kinases | Patients | Cancer therapies | Signal transduction | Gene amplification | Medical prognosis | Biomarkers | Hypoxia | Mutation | Tumors | Apoptosis
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16. Full Text Intracellular pH measured by31P-MR-spectroscopy might predict site of progression in recurrent glioblastoma under antiangiogenic therapy
: Intracellular pH Measured by31P-MR-S
by Wenger, Katharina J and Hattingen, Elke and Franz, Kea and Steinbach, Joachim P and Bähr, Oliver and Pilatus, Ulrich
Journal of Magnetic Resonance Imaging, ISSN 1053-1807, 10/2017, Volume 46, Issue 4, pp. 1200 - 1208
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17. Full Text Myoinositol as a Biomarker in Recurrent Glioblastoma Treated with Bevacizumab: A .sup.1H-Magnetic Resonance Spectroscopy Study
by Steidl, Eike and Pilatus, Ulrich and Hattingen, Elke and Steinbach, Joachim P and Zanella, Friedhelm and Ronellenfitsch, Michael W and Bahr, Oliver
PLoS ONE, ISSN 1932-6203, 12/2016, Volume 11, Issue 12, p. e0168113
Antiangiogenic treatment of glioblastomas with Bevacizumab lacks predictive markers. Myoinositol (MI) is an organic osmolyte, with intracellular concentration... 
Measurement | Inositol | Patient outcomes | Physiological aspects | Research | Drug therapy | Glioblastoma multiforme
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18. Full Text Erratum to: Gliomatosis cerebri: no evidence for a separate brain tumor entity
by Herrlinger, Ulrich and Jones, David T. W and Glas, Martin and Hattingen, Elke and Gramatzki, Dorothee and Stuplich, Moritz and Felsberg, Jörg and Bähr, Oliver and Gielen, Gerrit H and Simon, Matthias and Wiewrodt, Dorothee and Schabet, Martin and Hovestadt, Volker and Capper, David and Steinbach, Joachim P and von Deimling, Andreas and Lichter, Peter and Pfister, Stefan M and Weller, Michael and Reifenberger, Guido
Acta Neuropathologica, ISSN 0001-6322, 2/2016, Volume 131, Issue 2, pp. 321 - 322
Erratum to: Acta Neuropathol DOI 10.1007/s00401‑015‑1495‑z. The original version of this article contained errors in the alignment of several entries in Tables... 
Medicine & Public Health | Pathology | Neurosciences | Brain | Analysis | Brain tumors
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19. Full Text CASP9 germline mutation in a family with multiple brain tumors
: Familial Tumor Syndrome with CASP9 Germline Mutations
by Ronellenfitsch, Michael W and Oh, Ji-Eun and Satomi, Kaishi and Sumi, Koichiro and Harter, Patrick N and Steinbach, Joachim P and Felsberg, Jörg and Capper, David and Voegele, Catherine and Durand, Geoffroy and McKay, James and Le Calvez-Kelm, Florence and Schittenhelm, Jens and Klink, Barbara and Mittelbronn, Michel and Ohgaki, Hiroko
Brain Pathology, ISSN 1015-6305, 01/2018, Volume 28, Issue 1, pp. 94 - 102
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20. Full Text Tp53-induced glycolysis and apoptosis regulator (TIGAR) protects glioma cells from starvation-induced cell death by up-regulating respiration and improving cellular redox homeostasis
by Wanka, Christina and Steinbach, Joachim P and Rieger, Johannes
Journal of Biological Chemistry, ISSN 0021-9258, 09/2012, Volume 287, Issue 40, pp. 33436 - 33446
Altered metabolism in tumor cells is increasingly recognized as a core component of the neoplastic phenotype. Because p53 has emerged as a master metabolic... 
TKTL1 | TUMOR HYPOXIA | CANCER CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | KINASE | GLUCOSE METABOLITES | RECEPTOR | MUTATIONS | EXPRESSION | P53 | Cell Line | Reactive Oxygen Species | Oxidation-Reduction | Humans | Gene Expression Regulation | Gene Expression Regulation, Neoplastic | Oxygen Consumption | Intracellular Signaling Peptides and Proteins - metabolism | Brain Neoplasms - metabolism | Tumor Suppressor Protein p53 - genetics | Glioma - metabolism | Hypoxia - metabolism | Animals | Models, Biological | Cell Death | Cell Line, Tumor | Glycolysis | Mice | Intracellular Signaling Peptides and Proteins - physiology | Pentose Phosphate Pathway | Apoptosis | TIGAR | Glioma | Cell Metabolism | Pentose Pathway | Hypoxia | Metabolism | p53
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