M Weller

Summary

Country: Germany

Publications

  1. ncbi Enzastaurin-induced apoptosis in glioma cells is caspase-dependent and inhibited by BCL-XL
    Johannes Rieger
    Laboratory of Molecular Neuro Oncology, Department of General Neurology, University of Tubingen, Tubingen, Germany
    J Neurochem 106:2436-48. 2008
  2. ncbi Vertebral artery dissection presenting with ispilateral acute C5 and C6 sensorimotor radiculopathy: A case report
    Ghazaleh Tabatabai
    Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tubingen, Germany
    Cases J 1:139. 2008
  3. ncbi Glucocorticoid treatment of primary CNS lymphoma
    M Weller
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, Germany
    J Neurooncol 43:237-9. 1999
  4. ncbi Predicting chemoresistance in human malignant glioma cells: the role of molecular genetic analyses
    M Weller
    Department of Neurology, University of Tubingen, Germany
    Int J Cancer 79:640-4. 1998
  5. ncbi Elevated CSF lactoferrin in superficial siderosis of the central nervous system
    M Weller
    Department of Neurology, University of Tubingen, Medical School, Hoppe Seyler Strasse 3, D 72076 Tubingen, Germany
    J Neurol 246:943-5. 1999
  6. ncbi CD95 ligand-induced apoptosis of human medulloblastoma cells
    M Weller
    Department of Neurology, University of Tubingen, Medical School, Germany
    Cancer Lett 128:121-6. 1998
  7. ncbi [Neurooncology]
    M Weller
    Zentrum Onkologie, Abteilung Allgemeine Neurologie, Universitatsklinikum Tubingen
    Nervenarzt 74:1139-49. 2003
  8. ncbi Neuro-Oncology Working Group 01 trial of nimustine plus teniposide versus nimustine plus cytarabine chemotherapy in addition to involved-field radiotherapy in the first-line treatment of malignant glioma
    Michael Weller
    Department of Neurology, University of Tubingen, Medical School, Hoppe Seyler Strasse 3, 72076 Tubingen, Germany
    J Clin Oncol 21:3276-84. 2003
  9. ncbi Humoral immune response to p53 in malignant glioma
    M Weller
    Neurologische Klinik, Universitat Tubingen, Germany
    J Neurol 245:169-72. 1998
  10. ncbi CD95 ligand: lethal weapon against malignant glioma?
    M Weller
    Department of Neurology, University of Tubingen, Germany
    Brain Pathol 8:285-93. 1998

Collaborators

Detail Information

Publications150 found, 100 shown here

  1. ncbi Enzastaurin-induced apoptosis in glioma cells is caspase-dependent and inhibited by BCL-XL
    Johannes Rieger
    Laboratory of Molecular Neuro Oncology, Department of General Neurology, University of Tubingen, Tubingen, Germany
    J Neurochem 106:2436-48. 2008
    ..In ENZA-resistant A172 cells, apoptosis ligand 2 (Apo2L.0)-induced cleavage of caspases 3, 8, and 9 was increased by ENZA, resulting in synergistic activity of ENZA and Apo2L.0...
  2. ncbi Vertebral artery dissection presenting with ispilateral acute C5 and C6 sensorimotor radiculopathy: A case report
    Ghazaleh Tabatabai
    Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tubingen, Germany
    Cases J 1:139. 2008
    ..These symptoms completely resolved after anticoagulation and physical therapy...
  3. ncbi Glucocorticoid treatment of primary CNS lymphoma
    M Weller
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, Germany
    J Neurooncol 43:237-9. 1999
    ..Further, long-term glucocorticoid treatment is contraindicated in immunocompromised patients with primary CNS lymphoma...
  4. ncbi Predicting chemoresistance in human malignant glioma cells: the role of molecular genetic analyses
    M Weller
    Department of Neurology, University of Tubingen, Germany
    Int J Cancer 79:640-4. 1998
    ..We conclude that some important molecular changes, which are involved in the development of gliomas and attributed a role in regulating vulnerability to apoptosis, may not determine the response to chemotherapy in these tumors...
  5. ncbi Elevated CSF lactoferrin in superficial siderosis of the central nervous system
    M Weller
    Department of Neurology, University of Tubingen, Medical School, Hoppe Seyler Strasse 3, D 72076 Tubingen, Germany
    J Neurol 246:943-5. 1999
    ..Enhanced CSF lactoferrin may reflect an increased iron transport requirement in the central nervous system in superficial siderosis and might be a useful measure for monitoring response to therapy...
  6. ncbi CD95 ligand-induced apoptosis of human medulloblastoma cells
    M Weller
    Department of Neurology, University of Tubingen, Medical School, Germany
    Cancer Lett 128:121-6. 1998
    ..Interestingly, medulloblastoma cells belong to an increasing number of tumor cell types that coexpress CD95 and CD95L. We conclude that CD95 may be a promising target of immunochemotherapy for human medulloblastoma...
  7. ncbi [Neurooncology]
    M Weller
    Zentrum Onkologie, Abteilung Allgemeine Neurologie, Universitatsklinikum Tubingen
    Nervenarzt 74:1139-49. 2003
    ....
  8. ncbi Neuro-Oncology Working Group 01 trial of nimustine plus teniposide versus nimustine plus cytarabine chemotherapy in addition to involved-field radiotherapy in the first-line treatment of malignant glioma
    Michael Weller
    Department of Neurology, University of Tubingen, Medical School, Hoppe Seyler Strasse 3, 72076 Tubingen, Germany
    J Clin Oncol 21:3276-84. 2003
    ....
  9. ncbi Humoral immune response to p53 in malignant glioma
    M Weller
    Neurologische Klinik, Universitat Tubingen, Germany
    J Neurol 245:169-72. 1998
    ..These preliminary findings raise the possibility of systemic humoral immune responses to antigens, including mutant p53, expressed by glioma cells in the central nervous system...
  10. ncbi CD95 ligand: lethal weapon against malignant glioma?
    M Weller
    Department of Neurology, University of Tubingen, Germany
    Brain Pathol 8:285-93. 1998
    ..Although several issues regarding glioma cell sensitivity to CD95L/CD95-mediated apoptosis await elucidation, CD95 is a promising target for the treatment of malignant glioma...
  11. ncbi Combined 1p/19q loss in oligodendroglial tumors: predictive or prognostic biomarker?
    Michael Weller
    Department of General Neurology, University of Tubingen, Tubingen, Germany
    Clin Cancer Res 13:6933-7. 2007
    ..Importantly, the possible effect of combined 1p/19q loss has not been studied in patients who were not treated with radiotherapy or chemotherapy...
  12. ncbi Temozolomide: a milestone in the pharmacotherapy of brain tumors
    Michael Weller
    University of Tubingen Medical School, Department of General Neurology, Hertie Institute for Clinical Brain Research, Hoppe Seyler Strasse 3, Tubingen, Germany
    Future Oncol 1:747-54. 2005
    ..The early preliminary evidence for activity in recurrent malignant gliomas further resulted in a broad evaluation of TMZ for other tumors in neuro-oncology, mainly low-grade gliomas, brain metastases and primary cerebral lymphomas...
  13. ncbi [Standards and new developments in the chemotherapy of glioblastomas]
    M Weller
    Hertie Institut für Klinische Hirnforschung, Abteilung Allgemeine Neurologie, Zentrum Neurologie, Universitatsklinikum Tubingen
    Dtsch Med Wochenschr 130:2270-4. 2005
    ..EORTC 26 981/22 981/NCIC CE.3 thus defines a milestone in the treatment of glioblastoma and will provide a platform for further efforts at improving the outcome for patients suffering from this still invariably fatal neoplasm...
  14. ncbi Chimeric tumor suppressor 1, a p53-derived chimeric tumor suppressor gene, kills p53 mutant and p53 wild-type glioma cells in synergy with irradiation and CD95 ligand
    U Naumann
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, Institute of Pathology, , Hoppe-Seyler-Strasse 3, , Germany
    Cancer Res 61:5833-42. 2001
    ..CTS1 gene transfer is a promising strategy of somatic gene therapy for malignant glioma...
  15. ncbi Ezrin-dependent promotion of glioma cell clonogenicity, motility, and invasion mediated by BCL-2 and transforming growth factor-beta2
    W Wick
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, Tubingen, Germany
    J Neurosci 21:3360-8. 2001
    ....
  16. ncbi Glutathione depletion and neuronal cell death: the role of reactive oxygen intermediates and mitochondrial function
    U Wullner
    Department of Neurology, Eberhard Karls University, Hoppe Seyler Str 3, D 72076, Tubingen, Germany
    Brain Res 826:53-62. 1999
    ..No typical features of apoptosis, i.e., no chromatin condensation or DNA fragmentation were detected after GSH depletion after BSO or EA treatment...
  17. ncbi CCNU-dependent potentiation of TRAIL/Apo2L-induced apoptosis in human glioma cells is p53-independent but may involve enhanced cytochrome c release
    T A Röhn
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, Medical School, Tubingen, Germany
    Oncogene 20:4128-37. 2001
    ..These data provide novel insights into the role of the TRAIL/Apo2L system in malignant gliomas and illustrate that TRAIL/Apo2L-based immunochemotherapy may be an effective therapeutic strategy for these lethal neoplasms...
  18. ncbi Chemotherapy-induced cell death in primary cerebellar granule neurons but not in astrocytes: in vitro paradigm of differential neurotoxicity
    Antje Wick
    Laboratory of Molecular Neurodegeneration, Department of General Neurology and Hertie Institute for Clinical Brain Research, , Germany
    J Neurochem 91:1067-74. 2004
    ..zVAD-fmk, a caspase inhibitor and brain-derived neurotrophic factor (BDNF), but not MK-801, a non-competitive NMDA receptor antagonist, significantly reduced vincristine- or topotecan-induced cell death...
  19. ncbi Interferon-beta enhances monocyte and dendritic cell expression of B7-H1 (PD-L1), a strong inhibitor of autologous T-cell activation: relevance for the immune modulatory effect in multiple sclerosis
    Bettina Schreiner
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Hoppe Seyler Strasse 3, 72076 Tubingen, Germany
    J Neuroimmunol 155:172-82. 2004
    ..IFN-beta up-regulates B7-H1 in vitro and in MS patients in vivo and might represent a novel mechanism how IFN-beta acts as a negative modulator on APC T-cell interactions in the periphery...
  20. ncbi Lovastatin and phenylacetate induce apoptosis, but not differentiation, in human malignant glioma cells
    F Schmidt
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , School of Medicine, Hoppe-Seyler-Strasse 3, , Germany
    Acta Neuropathol 101:217-24. 2001
    ..We conclude that neoplastic glioma cells as well as untransformed rat astrocytes are refractory to the induction of differentiation by lovastatin and phenylacetate...
  21. ncbi APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis
    W Roth
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , , Germany
    Cell Death Differ 8:403-10. 2001
    ..These findings suggest that APRIL is involved in the regulation of death ligand-induced apoptotic signaling in malignant glioma cells...
  22. ncbi Boswellic acids and malignant glioma: induction of apoptosis but no modulation of drug sensitivity
    T Glaser
    Department of Neurology, , Germany
    Br J Cancer 80:756-65. 1999
    ..Further studies in laboratory animals and in human patients are required to determine whether boswellic acids may be a useful adjunct to the medical management of human malignant glioma...
  23. ncbi Primary central nervous system lymphoma 1991-1997: outcome and late adverse effects after combined modality treatment
    U Herrlinger
    Department of Neurology, University of Tuebingen, Tuebingen, Germany
    Cancer 91:130-5. 2001
    ....
  24. ncbi C2-ceramide signaling in glioma cells: synergistic enhancement of CD95-mediated, caspase-dependent apoptosis
    B Wagenknecht
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , , Germany
    Cell Death Differ 8:595-602. 2001
    ....
  25. ncbi Alkylphosphocholine-induced glioma cell death is BCL-X(L)-sensitive, caspase-independent and characterized by massive cytoplasmic vacuole formation
    U Naumann
    Laboratory of Molecular Neuro Oncology, Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Cell Death Differ 11:1326-41. 2004
    ..APC thus induce a characteristic morphological, BCL-X(L)-sensitive, apparently caspase-independent cell death involving mitochondrial alterations selectively in neoplastic astrocytic cells...
  26. ncbi Sublethal irradiation promotes migration and invasiveness of glioma cells: implications for radiotherapy of human glioblastoma
    C Wild-Bode
    Department of Neurology, , Medical School, Germany
    Cancer Res 61:2744-50. 2001
    ....
  27. ncbi CD95/CD95 ligand-independent potentiation of treosulfan cytotoxicity by BSO in malignant glioma cells in vitro and in vivo
    W Wick
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, D 72076 Tubingen, Germany
    Int J Oncol 21:213-20. 2002
    ..The glutathione levels in the non-tumor-bearing contralateral hemisphere were unaffected by systemic BSO treatment. The main side effects of treosulfan, gastrointestinal and bone marrow toxicity, were not significantly enhanced by BSO...
  28. ncbi N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast) inhibits transforming growth factor-beta relesase and reduces migration and invasiveness of human malignant glioma cells
    M Platten
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , School of Medicine, , Germany
    Int J Cancer 93:53-61. 2001
    ....
  29. ncbi Death receptor-independent cytochrome c release and caspase activation mediate thymidine kinase plus ganciclovir-mediated cytotoxicity in LN-18 and LN-229 human malignant glioma cells
    T Glaser
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , , Germany
    Gene Ther 8:469-76. 2001
    ..TK/GCV-mediated sensitization of glioma cells to CD95L expressed on immune effector cells or parenchymal brain cells might account for the immune system's and bystander effects of TK/GCV therapy observed in rodent glioma models in vivo...
  30. ncbi PCTAIRE3: a putative mediator of growth arrest and death induced by CTS-1, a dominant-positive p53-derived synthetic tumor suppressor, in human malignant glioma cells
    U Naumann
    Laboratory of Molecular Neuro Oncology, Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Cancer Gene Ther 13:469-78. 2006
    ..Altogether, these data identify PCTAIRE3 as one novel growth-inhibitory and death-inducing p53 response gene and suggest that changes in the expression of specific target genes contribute to the superior anti-glioma activity of CTS-1...
  31. ncbi Taxol-mediated augmentation of CD95 ligand-induced apoptosis of human malignant glioma cells: association with bcl-2 phosphorylation but neither activation of p53 nor G2/M cell cycle arrest
    W Roth
    Department of Neurology, , School of Medicine, Germany
    Br J Cancer 77:404-11. 1998
    ....
  32. ncbi Topoisomerase-I inhibitors for human malignant glioma: differential modulation of p53, p21, bax and bcl-2 expression and of CD95-mediated apoptosis by camptothecin and beta-lapachone
    M Weller
    Department of Neurology, University of Tubingen, Medical School, Germany
    Int J Cancer 73:707-14. 1997
    ..Camptothecin-like agents are particularly promising for immunochemotherapy of malignant glioma using cytotoxic drugs and CD95 ligand...
  33. ncbi Secreted Frizzled-related proteins inhibit motility and promote growth of human malignant glioma cells
    W Roth
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, Hoppe Seyler Strasse 3, 72076 Tubingen, Germany
    Oncogene 19:4210-20. 2000
    ..These data support a function for Wnt signaling and its modulation by sFRPs in the biology of human gliomas. Oncogene (2000) 19, 4210 - 4220..
  34. ncbi Adenoviral expression of XIAP antisense RNA induces apoptosis in glioma cells and suppresses the growth of xenografts in nude mice
    U Naumann
    Laboratory of Molecular Neuro Oncology, Department of General Neurology, Hertie Institute for Clinical Brain Research, Tubingen, Germany
    Gene Ther 14:147-61. 2007
    ..Altogether, these data define a powerful survival function for XIAP and reinforce its possible role as a therapeutic target in human glioma cells...
  35. ncbi One week on/one week off: a novel active regimen of temozolomide for recurrent glioblastoma
    W Wick
    Department of General Neurology, Hertie Institute for Clinical Brain Research, , Germany
    Neurology 62:2113-5. 2004
    ..Two patients achieved a partial response (10%), and 17 patients (81%) had stable disease. The median progression-free survival was 5 months. The progression-free survival at 6 months was 48%...
  36. ncbi BCL-2 family protein expression in initial and recurrent glioblastomas: modulation by radiochemotherapy
    H Strik
    Institute of Brain Research, Medical School, Tubingen, Germany
    J Neurol Neurosurg Psychiatry 67:763-8. 1999
    ..The differences of expression of BCL-2, BCL-X, BAX, and MCL-1 proteins of paired first resection and recurrence glioblastoma specimens were examined...
  37. ncbi Neuroprotection by hypoxic preconditioning requires sequential activation of vascular endothelial growth factor receptor and Akt
    Antje Wick
    Laboratory of Neurodegeneration, Department of Neurology, , , Germany
    J Neurosci 22:6401-7. 2002
    ..Our data are indicating a sequential requirement for VEGF/VEGFR-2 activation and Akt/PKB phosphorylation for neuronal survival mediated by hypoxic preconditioning and propose VEGF as a hypoxia-induced neurotrophic factor...
  38. ncbi Cilengitide modulates attachment and viability of human glioma cells, but not sensitivity to irradiation or temozolomide in vitro
    Gabriele D Maurer
    Department of Neurology, University Hospital of Tubingen, Hertie Institute for Clinical Brain Research, Tubingen, Germany
    Neuro Oncol 11:747-56. 2009
    ..These data suggest that the beneficial clinical effects derived from cilengitide in vivo may arise from altered perfusion, which promotes temozolomide delivery to glioma cells...
  39. ncbi MICA/NKG2D-mediated immunogene therapy of experimental gliomas
    Manuel A Friese
    Department of Neurology, , , Germany
    Cancer Res 63:8996-9006. 2003
    ..These data commend MICA immunogene therapy as a novel experimental treatment for human malignant gliomas...
  40. ncbi Expression and functional activity of osteoprotegerin in human malignant gliomas
    U Naumann
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen Medical School, Auf der Morgenstelle 15, 72076, Tubingen, Germany
    Acta Neuropathol 107:17-22. 2004
    ..Altogether, however, these data suggest that OPG expression may not be a major pathway of glioma cell resistance to future Apo2L/TRAIL-based therapeutic approaches...
  41. ncbi Glioma cell invasion: regulation of metalloproteinase activity by TGF-beta
    W Wick
    Department of Neurology, University of Tubingen, Germany
    J Neurooncol 53:177-85. 2001
    ..By virtue of its promotion of glioma invasion and its growth regulatory and immunomodulatory properties. TGF-beta continues to be one of the most promising targets for the experimental therapy of human malignant glioma...
  42. ncbi A novel p53 rescue compound induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis
    L Weinmann
    Laboratory of Molecular Neuro Oncology, Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen School of Medicine, Tubingen D 72076, Germany
    Cell Death Differ 15:718-29. 2008
    ..0 are sensitive to siRNA-mediated downregulation of p53. Thus this new p53 rescue compound may open up novel perspectives for the treatment of cancers currently considered resistant to the therapeutic induction of apoptosis...
  43. ncbi Processing of immunosuppressive pro-TGF-beta 1,2 by human glioblastoma cells involves cytoplasmic and secreted furin-like proteases
    J Leitlein
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , , Germany
    J Immunol 166:7238-43. 2001
    ..Thus, subtilisin-like proprotein convertases may represent a novel target for the immunotherapy of malignant glioma and other cancers or pathological conditions characterized by enhanced TGF-beta bioactivity...
  44. ncbi Dual effect of glucocorticoids on apoptosis of human autoreactive and foreign antigen-specific T cells
    F Zipp
    Department of Neurology, Division of Neuroimmunology, University Hospital Charite, Campus Mitte, NWFZ, Geb 2680, R 04023, Schumann Strasse 20 21, 10117, Berlin, Germany
    J Neuroimmunol 110:214-22. 2000
    ....
  45. ncbi Serum CD95 of relapsing remitting multiple sclerosis patients protects from CD95-mediated apoptosis
    F Zipp
    Department of Neurology, University of Tubingen, Germany
    J Neuroimmunol 86:151-4. 1998
    ..Thus, MS sera contain biologically active inhibitors of T cell apoptosis that may allow for prolonged abnormal immune responses...
  46. ncbi CD95 expression and CD95-mediated apoptosis of T cells in multiple sclerosis. No differences from normal individuals and no relation to HLA-DR2
    F Zipp
    Department of Neurology, University of Tubingen, Germany
    J Neuroimmunol 81:168-72. 1998
    ..However, to assess the contribution of T cell apoptosis to the pathogenesis of MS further studies on other details of the complex system leading to T cell apoptosis are required...
  47. ncbi High level expression of expanded full-length ataxin-3 in vitro causes cell death and formation of intranuclear inclusions in neuronal cells
    B O Evert
    Department of Neurology, University of Tubingen, 72076 Tubingen, Germany
    Hum Mol Genet 8:1169-76. 1999
    ..These data show that high level expression of expanded full-length ataxin-3 in a neuron-like cell line generates ultrastructural alterations of SCA3 pathogenesis and results in increased spontaneous non-apoptotic cell death...
  48. ncbi Extended therapeutic window for caspase inhibition and synergy with MK-801 in the treatment of cerebral histotoxic hypoxia
    J B Schulz
    Experimental Neuropharmacology Laboratory, Department of Neurology, University of Tubingen, Hoppe Seyler Str 3, D 72076 Tubingen
    Cell Death Differ 5:847-57. 1998
    ..They strongly implicate early excitotoxicity and delayed caspase activation in neuronal loss after focal ischemic lesions and offer a new strategy for the treatment of stroke...
  49. ncbi Identification of p21 as a target of cycloheximide-mediated facilitation of CD95-mediated apoptosis in human malignant glioma cells
    T Glaser
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , , Germany
    Oncogene 20:4757-67. 2001
    ....
  50. ncbi Expression of the B7-related molecule ICOSL by human glioma cells in vitro and in vivo
    Bettina Schreiner
    Department of Neurology, University of Tubingen, Medical School, Tubingen, Germany
    Glia 44:296-301. 2003
    ..However, ICOSL gene transfer into glioma cells does not alter their immunogenicity under primary or secondary alloreactive coculture assays...
  51. ncbi Monocyte-derived HLA-G acts as a strong inhibitor of autologous CD4 T cell activation and is upregulated by interferon-beta in vitro and in vivo: rationale for the therapy of multiple sclerosis
    Meike Mitsdoerffer
    Department of Neurology, University of Tubingen, Hoppe Seyler Strasse 3, D 72076 Tubingen, Germany
    J Neuroimmunol 159:155-64. 2005
    ..We conclude that some desirable immune-modulatory effects of INF-beta might be accomplished via the upregulation of the immune-tolerogenic molecule HLA-G...
  52. ncbi NOA-04 randomized phase III trial of sequential radiochemotherapy of anaplastic glioma with procarbazine, lomustine, and vincristine or temozolomide
    Wolfgang Wick
    Department of Neurology and Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    J Clin Oncol 27:5874-80. 2009
    ..The NOA-04 phase III trial compared efficacy and safety of radiotherapy followed by chemotherapy at progression with the reverse sequence in patients with newly diagnosed anaplastic gliomas...
  53. ncbi Irradiation and hypoxia promote homing of haematopoietic progenitor cells towards gliomas by TGF-beta-dependent HIF-1alpha-mediated induction of CXCL12
    Ghazaleh Tabatabai
    Laboratory of Molecular Neuro-Oncology, , , Germany
    Brain 129:2426-35. 2006
    ..These data suggest that the use of HPC as cellular vectors in the treatment of glioblastoma may well be combined with irradiation or other anti-angiogenic therapies that induce tumour hypoxia...
  54. ncbi Preirradiation gemcitabine chemotherapy for newly diagnosed glioblastoma. A phase II study
    M Weller
    Department of Neurology, University of Tubingen Medical School, Tubingen, Germany
    Cancer 91:423-7. 2001
    ..To improve the outcome for glioblastoma patients, the authors evaluated the therapeutic efficacy of preirradiation gemcitabine chemotherapy followed by standard radiotherapy...
  55. ncbi Adult medulloblastoma: prognostic factors and response to therapy at diagnosis and at relapse
    Ulrich Herrlinger
    Department of Neurology, Hertie Institute for Clinical Brain Research University of Tübingen Medical School, Hoppe Seyler Str 3, 72076 Tubingen, Germany
    J Neurol 252:291-9. 2005
    ..Moreover, second-line therapy may be beneficial for these patients. As in pediatric medulloblastoma patients, primary infiltration of the floor of the 4(th) ventricle indicates a poor prognosis...
  56. ncbi Endonucleolytic DNA fragmentation is not required for apoptosis of cultured rat cerebellar granule neurons
    J B Schulz
    Department of Neurology, University of Tubingen, Germany
    Neurosci Lett 245:9-12. 1998
    ....
  57. ncbi Molecular determinants of glioma cell migration and invasion
    C Wild-Bode
    Department of Neurology, , School of Medicine, Germany
    J Neurosurg 94:978-84. 2001
    ..Antiapoptotic BCL-2 family protein expression is a predictor of efficient migration and invasion...
  58. ncbi Identification by suppression subtractive hybridization of p21 as a radio-inducible gene in human glioma cells
    A Rimner
    Department of Neurology, , School of Medicine, Germany
    Anticancer Res 21:3505-8. 2001
    ..We conclude that the identification of radio-inducible genomic sequences suitable for radio-gene therapy may turn out to be difficult...
  59. ncbi Adenoviral natural born killer gene therapy for malignant glioma
    Ulrike Naumann
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, D 72076 Tubingen, Germany
    Hum Gene Ther 14:1235-46. 2003
    ..Thus Ad-NBK triggers an XIAP- and zVAD-fmk-sensitive cell death pathway in glioma cells with potential therapeutic value, provided that NBK expression can be selectively targeted to cancer cells...
  60. ncbi Expression of the B7-related molecule B7-H1 by glioma cells: a potential mechanism of immune paralysis
    Sabine Wintterle
    Department of Neurology, Medical School, , Hoppe-Seyler-Strasse 3, , Germany
    Cancer Res 63:7462-7. 2003
    ..B7-H1 expression may thus significantly influence the outcome of T-cell tumor cell interactions and represents a novel mechanism by which glioma cells evade immune recognition and destruction...
  61. ncbi Human malignant glioma cells express semaphorins and their receptors, neuropilins and plexins
    Johannes Rieger
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, Tubingen, Germany
    Glia 42:379-89. 2003
    ....
  62. ncbi RNA interference targeting transforming growth factor-beta enhances NKG2D-mediated antiglioma immune response, inhibits glioma cell migration and invasiveness, and abrogates tumorigenicity in vivo
    Manuel A Friese
    Department of General Neurology, Hertie Institute for Clinical Brain Research and Institute for Cell Biology, Department of Immunology, , , Germany
    Cancer Res 64:7596-603. 2004
    ....
  63. ncbi Modulation of TGF-beta activity by latent TGF-beta-binding protein 1 in human malignant glioma cells
    Isabel Tritschler
    Department of General Neurology, Laboratory of Molecular Neuro Oncology, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    Int J Cancer 125:530-40. 2009
    ..Collectively, we identify LTBP-1 as an important modulator of TGF-beta activation in glioma cells, which may contribute to the malignant phenotype of these tumors...
  64. ncbi FasL (CD95L/APO-1L) resistance of neurons mediated by phosphatidylinositol 3-kinase-Akt/protein kinase B-dependent expression of lifeguard/neuronal membrane protein 35
    Christoph P Beier
    Department of Neurology, Medical School, University of Tubingen, 72076 Tubingen, Germany
    J Neurosci 25:6765-74. 2005
    ..These results demonstrate that LFG mediated the FasL resistance of CGNs and that, under certain circumstances, e.g., inhibition of the PI 3-kinase-Akt/PKB pathway, CGNs were sensitized to FasL...
  65. ncbi Supraagonistic, bispecific single-chain antibody purified from the serum of cloned, transgenic cows induces T-cell-mediated killing of glioblastoma cells in vitro and in vivo
    Ludger Grosse-Hovest
    Institute for Cell Biology, Department of Immunology, , , Germany
    Int J Cancer 117:1060-4. 2005
    ....
  66. ncbi Diva/Boo is a negative regulator of cell death in human glioma cells
    U Naumann
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, Hoppe Seyler Str 3, D 72076 Tubingen, Germany
    FEBS Lett 505:23-6. 2001
    ....
  67. ncbi Primary central nervous system lymphomas (PCNSL): MRI response criteria revised
    W Kuker
    Department of Neuroradiology, Medical School, University of Tubingen, Berlin, Germany
    Neurology 65:1129-31. 2005
    ..Because contrast enhancement may not necessarily indicate residual, biologically active lymphoma, the authors propose a modification of the Macdonald response criteria...
  68. ncbi PCV chemotherapy for recurrent glioblastoma
    F Schmidt
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, Medical School, Tuebingen, Germany
    Neurology 66:587-9. 2006
    ..Median progression-free survival was 17.1 weeks and progression-free survival at 6 months was 38.4%. World Health Organization grade III/IV hematologic toxicity was common (25.6%), but nonhematologic toxicity was mild...
  69. ncbi Surviving glioblastoma for more than 5 years: the patient's perspective
    J P Steinbach
    Department of General Neurology, Hertie Institute for Clinical Brain Research, Tubingen, Germany
    Neurology 66:239-42. 2006
    ..Depression and anxiety were common. Although most patients thought that their social functioning and work ability were impaired, little reduction in overall quality of life was perceived...
  70. ncbi Phase II trial of lomustine plus temozolomide chemotherapy in addition to radiotherapy in newly diagnosed glioblastoma: UKT-03
    Ulrich Herrlinger
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    J Clin Oncol 24:4412-7. 2006
    ..To evaluate toxicity and efficacy of the combination of lomustine, temozolomide (TMZ) and involved-field radiotherapy in patients with newly diagnosed glioblastoma (GBM)...
  71. ncbi WHO grade associated downregulation of MHC class I antigen-processing machinery components in human astrocytomas: does it reflect a potential immune escape mechanism?
    Matthias Mehling
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Hoppe Seyler Strasse 3, 72076, Tubingen, Germany
    Acta Neuropathol 114:111-9. 2007
    ....
  72. ncbi Chemoradiotherapy of newly diagnosed glioblastoma with intensified temozolomide
    Markus Weiler
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Int J Radiat Oncol Biol Phys 77:670-6. 2010
    ..To evaluate the toxicity and efficacy of chemoradiotherapy with temozolomide (TMZ) administered in an intensified 1-week on/1-week off schedule plus indomethacin in patients with newly diagnosed glioblastoma...
  73. ncbi SD-208, a novel transforming growth factor beta receptor I kinase inhibitor, inhibits growth and invasiveness and enhances immunogenicity of murine and human glioma cells in vitro and in vivo
    Martin Uhl
    Laboratory of Molecular Neuro-Oncology, Department of General Neurology, Hertie Institute for Clinical Brain Research, , School of Medicine, , Germany
    Cancer Res 64:7954-61. 2004
    ..These data define TGF-beta receptor I kinase inhibitors such as SD-208 as promising novel agents for the treatment of human malignant glioma and other conditions associated with pathological TGF-beta activity...
  74. ncbi CP-31398, a novel p53-stabilizing agent, induces p53-dependent and p53-independent glioma cell death
    J Wischhusen
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, Medical School, , , Germany
    Oncogene 22:8233-45. 2003
    ....
  75. ncbi Identification of inhibitor-of-differentiation 2 (Id2) as a modulator of neuronal apoptosis
    M Gleichmann
    Department of Neurology, , , Germany
    J Neurochem 80:755-62. 2002
    ..Further, gene transfer- mediated overexpression of Id2 induces neuronal cell death both in high potassium and low potassium conditions. Thus, the present study defines a role for Id2 in the modulation of neuronal apoptosis...
  76. ncbi Heat shock protein expression in human gliomas
    H M Strik
    Institute of Brain Research, Medical School, University of Tubingen, Calwer Str 3, D 72076 Tubingen, Germany
    Anticancer Res 20:4457-62. 2000
    ..Here, we asked whether the differential response to radiochemotherapy and different overall prognosis for astrocytic and oligodendroglial tumours can be accounted for by differences in HSP expression...
  77. ncbi NF-kappaB-independent actions of sulfasalazine dissociate the CD95L- and Apo2L/TRAIL-dependent death signaling pathways in human malignant glioma cells
    M Hermisson
    Laboratory of Molecular Neuro-Oncology, Department of Neurology, , , Germany
    Cell Death Differ 10:1078-89. 2003
    ..Thus, SS modulates the death cascades triggered by CD95L and Apo2L/TRAIL in opposite directions in an NF-kappaB-independent manner, and SS may be a promising agent for the augmentation of Apo2L/TRAIL-based cancer therapies...
  78. ncbi Cell death and apoptosis regulating proteins in Parkinson's disease--a cautionary note
    U Wullner
    Department of Neurology, Friedrich Wilhelms University, Bonn, Germany
    Acta Neuropathol 97:408-12. 1999
    ..No significant changes of any of the apoptosis regulating proteins were apparent in PD substantia nigra. These findings do not support the hypothesis that apoptosis plays a central role in the pathogenesis of PD...
  79. ncbi Hypoxia-induced cell death in human malignant glioma cells: energy deprivation promotes decoupling of mitochondrial cytochrome c release from caspase processing and necrotic cell death
    J P Steinbach
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, Tubingen, Germany
    Cell Death Differ 10:823-32. 2003
    ..These findings suggest that glioma cells resist adverse effects of hypoxia until energy stores are depleted and then undergo necrosis rather than apoptosis because of energy deprivation...
  80. ncbi Apoptotic cell death in the cerebellum of mutant weaver and lurcher mice
    U Wullner
    Department of Neurology, Eberhard Karls University, Tubingen, Germany
    Neurosci Lett 200:109-12. 1995
    ..These mutant mice offer the opportunity to study the mechanisms that underlie inappropriate apoptotic cell death in vivo...
  81. ncbi EGR-1 is regulated by N-methyl-D-aspartate-receptor stimulation and associated with patient survival in human high grade astrocytomas
    Michel Mittelbronn
    Institute of Brain Research, University of Tubingen, Tubingen, Germany
    Brain Pathol 19:195-204. 2009
    ..The NMDA-R-mediated EGR-1 expression, therefore, seems to be a promising target for novel clinical approaches to astrocytoma treatment...
  82. ncbi Neoadjuvant gemcitabine/treosulfan chemotherapy for newly diagnosed glioblastoma: a phase II study
    Wolfgang Wick
    Department of Neurology, , Germany
    J Neurooncol 59:151-5. 2002
    ..The schedule used in the present study did not confer any significant survival advantage compared with standard involved field radiotherapy alone...
  83. ncbi BCL-2 family proteins modulate radiosensitivity in human malignant glioma cells
    Johannes R Streffer
    Department of Neurology, , Germany
    J Neurooncol 56:43-9. 2002
    ..Thus, BCL-2 family protein expression modulates radiosensitivity in human glioma cells and targeted alterations in BCL-2 family protein expression are a promising strategy to improve the therapeutic efficacy of radiotherapy for gliomas...
  84. ncbi Monocyte chemoattractant protein-1 increases microglial infiltration and aggressiveness of gliomas
    Michael Platten
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen Medical School, Hoppe Seyler Strasse 3, 72076 Tubingen, Germany
    Ann Neurol 54:388-92. 2003
    ..This provides the first functional evidence that MCP-1 recruits microglial cells to gliomas and promotes their growth in vivo. Microglial cells may support rather than suppress glioma growth...
  85. ncbi Expression of the immune-tolerogenic major histocompatibility molecule HLA-G in multiple sclerosis: implications for CNS immunity
    Heinz Wiendl
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Brain 128:2689-704. 2005
    ..This pathway may act as an inhibitory feedback aimed to downregulate the deleterious effects of T-cell infiltration in neuroinflammation...
  86. ncbi Central nervous system Hodgkin's lymphoma without systemic manifestation: case report and review of the literature
    U Herrlinger
    Department of Neurology, University of Tubingen, Germany
    Acta Neuropathol 99:709-14. 2000
    ..Moreover, EBV-encoded RNA-1 (EBER-1) sequences and a monoclonal rearrangement of the immunoglobulin heavy chain CDR2 locus were detected...
  87. ncbi Vascular endothelial growth factor (VEGF) in leptomeningeal metastasis: diagnostic and prognostic value
    U Herrlinger
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Hoppe Seyler Str 3, D 72076 Tuebingen, Germany
    Br J Cancer 91:219-24. 2004
    ..High VEGF levels have a very high specificity for LM and may help to establish the diagnosis. The role of VEGF as a predictor of outcome should be substantiated in prospective studies...
  88. ncbi N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast) suppresses microglial inducible nitric oxide synthase (iNOS) expression and activity induced by interferon-gamma (IFN-gamma)
    M Platten
    Laboratory of Molecular Neuro Oncology, Department of Neurology, University of Tubingen, School of Medicine, Hoppe Seyler Str 3, 72076 Tubingen, Germany
    Br J Pharmacol 134:1279-84. 2001
    ..5. These results suggest that tranilast-mediated suppression of microglial iNOS activity induced by IFN-gamma involves the inhibition of NF-kappaB-dependent iNOS mRNA expression...
  89. ncbi The role of caspases 9 and 9-short (9S) in death ligand- and drug-induced apoptosis in human astrocytoma cells
    Robert Waltereit
    Laboratory for Molecular Neuro Oncology, Department of Neurology, University of Tuebingen, Hoppe Seyler Str 3, Germany
    Brain Res Mol Brain Res 106:42-9. 2002
    ..We conclude that the expression levels of caspase 9 or caspase 9S do not play a major role in determining vulnerability to apoptosis in human astrocytoma cells...
  90. ncbi Migratory neural stem cells for improved thymidine kinase-based gene therapy of malignant gliomas
    Martin Uhl
    Department of General Neurology, Hertie Institute for Clinical Brain Research, , Hoppe-Seyler-Str. 3, , Germany
    Biochem Biophys Res Commun 328:125-9. 2005
    ..In conclusion, we delineate a role for migratory HSV-transfected NSC to eliminate glioma cells purely by means of the bystander effect...
  91. ncbi Defective p53 antiangiogenic signaling in glioblastoma
    Benjamin Berger
    Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany
    Neuro Oncol 12:894-907. 2010
    ..These data challenge the view of p53 as an angiogenesis-regulator in glioblastoma in that relevant signaling pathways are silenced, potentially contributing to the angiogenic switch during malignant progression...
  92. ncbi Lessons from the bone marrow: how malignant glioma cells attract adult haematopoietic progenitor cells
    Ghazaleh Tabatabai
    Department of General Neurology, Hertie Institute for Clinical Brain Research, , , Germany
    Brain 128:2200-11. 2005
    ..Thus, we define here the molecular mechanism underlying the glioma tropism of the probably most easily accessible PC population suitable for cancer therapy, that is, adult haematopoietic PC...
  93. ncbi ACNU-based chemotherapy for recurrent glioma in the temozolomide era
    Caroline Happold
    Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Medical School, Tubingen, Germany
    J Neurooncol 92:45-8. 2009
    ..This study does not commend ACNU as a therapy of first choice for patients with recurrent glioblastomas pretreated with temozolomide...
  94. ncbi Primary CNS lymphoma in the elderly: temozolomide therapy and MGMT status
    Delia Kurzwelly
    Division of Clinical Neurooncology, Department of Neurology, University of Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    J Neurooncol 97:389-92. 2010
    ..Temozolomide monotherapy appears to be effective in a subgroup of elderly PCNSL patients and deserves further evaluation...
  95. ncbi Aryl hydrocarbon receptor inhibition downregulates the TGF-beta/Smad pathway in human glioblastoma cells
    D Gramatzki
    Laboratory of Molecular Neuro Oncology, Department of General Neurology and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    Oncogene 28:2593-605. 2009
    ....
  96. ncbi First-line therapy with temozolomide induces regression of primary CNS lymphoma
    U Herrlinger
    Department of Neurology, University of Tuebingen, Germany
    Neurology 58:1573-4. 2002
  97. ncbi APO2 ligand: a novel lethal weapon against malignant glioma?
    J Rieger
    Department of Neurology, University of Tubingen, School of Medicine, Germany
    FEBS Lett 427:124-8. 1998
    ..APO2L targeting may be a promising approach for selectively targeting apoptosis to human malignant glioma cells...
  98. ncbi A novel tool to analyze MRI recurrence patterns in glioblastoma
    Wolfgang Wick
    Department of Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Neuro Oncol 10:1019-24. 2008
    ..The data show the feasibility of groupwise recurrence pattern analysis. An effect of TMZ treatment on the recurrence pattern in the EORTC 26981/22981/NCIC CE.3 study could not be demonstrated...
  99. ncbi Malignant glioma biology: role for TGF-beta in growth, motility, angiogenesis, and immune escape
    M Platten
    Department of Neurology, University of Tubingen, 72076 Tubingen, Germany
    Microsc Res Tech 52:401-10. 2001
    ..By virtue of its growth regulatory and immunomodulatory properties, TGF-beta promises to become a novel target for the experimental therapy of human malignant glioma...