Martina Deckert

University of Cologne, Köln, North Rhine-Westphalia, Germany

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Publications (130)671.97 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The role of the type 2 helper T cell (Th2)-polarizing cytokines IL-4 and IL-10 has not yet been studied in P0106-125-induced murine experimental autoimmune neuritis (EAN). We, therefore, addressed the functional relevance of these cytokines and signaling via the IL-4-associated transcription factor STAT6. The clinical course of P0106-125-induced EAN in mice deficient for IL-10(0/0), IL-4(0/0), or STAT6(0/0) was significantly aggravated compared with that of wild-type control mice. In addition, treatment of P0106-125-immunized C57BL/6 mice at the onset of clinical symptoms with a monoclonal IL-10 neutralizing antibody aggravated symptoms and prolonged disease to a similar degree as in IL-10(0/0) mice. This exacerbated course was attributed to a more prominent Th1 immune response associated with a persistent M1 milieu in the sciatic nerve and in the regional and systemic lymphatic system. These data suggest a Th2-polarized milieu being required to prevent axonal damage of the sciatic nerve and to terminate the P0106-125-specific immune response in EAN. Beyond the already known role of macrophages as pathogenic effector cells in EAN, these data suggest that M2-differentiated macrophages do not damage and may even protect neural tissues in EAN. Thus, these data highlight the pathogenetic relevance of the macrophage polarization status in EAN. Therapeutic modulation of immune responses from an M1 toward an M2 milieu may be a promising novel strategy in peripheral nervous system neuritis.
    The American journal of pathology. 08/2014;
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    ABSTRACT: Myelin protein 0 peptide 106-125-induced murine experimental autoimmune neuritis (EAN) is a CD4-positive T cell-mediated monophasic axonal inflammatory neuropathy; interferon-γ is the key proinflammatory mediator. Experimental autoimmune neuritis is well suited for elucidating pathogenetic mechanisms underlying human acute axonal Guillain-Barré syndrome. Here, the functional role of the costimulatory molecule CD40 was defined by characterization of EAN in CD40-deficient mice. In contrast to immunized C57BL/6 mice, CD40-deficient mice were resistant to EAN owing to impaired priming of CD4-positive T-effector cells. To determine whether CD40 is a suitable candidate for the treatment of EAN, we administered monoclonal anti-CD40 antibody either before immunization or upon onset of neurologic signs. Prophylactic anti-CD40 treatment completely abolished CD4-positive T-cell priming. Therapeutic application of anti-CD40 prevented full activation of CD4-positive T cells that were in the process of priming and suppressed production of interferon-γ in peripheral lymph nodes, spleen, and serum, and of interleukin-6, interleukin-12p40, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1, which are associated with activation of the nuclear factor-κB signaling pathway. This resulted in enhanced recovery by early generation of CD25-positive, Foxp3-positive, CD4-positive regulatory T cells. Thus, these experiments highlight the crucial role of CD40 as an important costimulatory molecule in EAN and suggest that it has potential as a therapeutic target in human neuritis.
    Journal of neuropathology and experimental neurology. 04/2014;
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    ABSTRACT: Primary lymphoma of the central nervous system (CNS, PCNSL) is a specific diffuse large B cell lymphoma entity arising in and confined to the CNS. Despite extensive research since many decades, the pathogenetic mechanisms underlying the remarkable tropism of this peculiar malignant hematopoietic tumor remain still to be elucidated. In the present review, we summarize the present knowledge on the genotypic and phenotypic characteristics of the tumor cells of PCNSL, give an overview over deregulated molecular pathways in PCNSL and present recent progress in the field of preclinical modeling of PCNSL in mice. With regard to the phenotype, PCNSL cells resemble late germinal center exit IgM+IgD+ B cells with blocked terminal B cell differentiation. They show continued BCL6 activity in line with ongoing activity of the germinal center program. This together with the pathways deregulated by genetic alterations may foster B cell activation and brisk proliferation, which correlated with the simultaneous MYC and BCL2 overexpression characteristic for PCNSL. On the genetic level, PCNSL are characterized by ongoing aberrant somatic hypermutation that, besides the IG locus, targets the PAX5, TTF, MYC, and PIM1 genes. Moreover, PCNSL cells show impaired IG class switch due to sμ region deletions, and PRDM1 mutations. Several important pathways, i.e., the B cell receptor (BCR), the toll-like receptor, and the nuclear factor-κB pathway, are activated frequently due to genetic changes affecting genes like CD79B, SHIP, CBL, BLNK, CARD11, MALT1, BCL2, and MYD88. These changes likely foster tumor cell survival. Nevertheless, many of these features are also present in subsets of systemic DLBLC and might not be the only reasons for the peculiar tropism of PCNSL. Here, preclinical animal models that closely mimic the clinical course and neuropathology of human PCNSL may provide further insight and we discuss recent advances in this field. Such models enable us to understand the pathogenetic interaction between the malignant B cells, resident cell populations of the CNS, and the associated inflammatory infiltrate. Indeed, the immunophenotype of the CNS as well as tumor cell characteristics and intracerebral interactions may create a micromilieu particularly conducive to PCNSL that may foster aggressiveness of tumor cells and accelerate the fatal course of disease. Suitable animal models may also serve as a well-defined preclinical system and may provide a useful tool for developing new specific therapeutic strategies.
    Acta Neuropathologica 11/2013; · 9.73 Impact Factor
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    ABSTRACT: Single-nucleotide polymorphisms in the tumor necrosis factor, alpha-induced protein 3 gene, which encodes the ubiquitin-modifying protein A20, are linked to susceptibility to multiple sclerosis (MS), a demyelinating autoimmune disease of the central nervous system (CNS). Since it is unresolved how A20 regulates MS pathogenesis, we examined its function in a murine model of MS, namely experimental autoimmune encephalomyelitis (EAE). Deletion of A20 in neuroectodermal cells (astrocytes, neurons, and oligodendrocytes; Nestin-Cre A20(fl/fl) mice) or selectively in astrocytes (GFAP-Cre A20(fl/fl) mice) resulted in more severe EAE as compared to control animals. In Nestin-Cre A20(fl/fl) and GFAP-Cre A20(fl/fl) mice demyelination and recruitment of inflammatory leukocytes were increased as compared to A20(fl/fl) control mice. Importantly, numbers of encephalitogenic CD4(+) T cells producing interferon (IFN)-γ, interleukin (IL)-17, and granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively, as well as mRNA production of IFN-γ, IL-17, tumor necrosis factor (TNF), GM-CSF, IL-6, CXCL1, CCL2, and CXCL10 were significantly increased in spinal cords of Nestin-Cre A20(fl/fl) and GFAP-Cre A20(fl/fl) mice, respectively. Compared to A20-sufficient astrocytes, A20-deficient astrocytes displayed stronger activation of nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) in response to TNF, IL-17, and GM-CSF, and of signal transducer and activator of transcription 1 (STAT1) upon IFN-γ stimulation. Due to NF-κB and STAT1 hyperactivation, A20-deficient astrocytes produced significantly more chemokines in response to these key encephalitogenic cytokines of autoimmune CD4(+) T cells resulting in an amplification of CD4(+) T cell recruitment to the CNS. Thus, astrocytic A20 is an important inhibitor of autoimmune-mediated demyelination in the CNS.
    Acta Neuropathologica 09/2013; · 9.73 Impact Factor
  • Acta Neuropathologica 09/2013; · 9.73 Impact Factor
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    ABSTRACT: Primary lymphoma of the central nervous system is a distinct diffuse large B-cell lymphoma confined to the nervous system. Whereas classical cases can be classified easily, differential diagnosis can be a challenge in particular in patients who had received treatment prior to biopsy. In the differential diagnosis, other tumours and inflammatory diseases of autoimmune and infectious aetiology need to be considered. Copyright © 2013 John Wiley & Sons, Ltd.
    Hematological Oncology 08/2013; · 2.04 Impact Factor
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    ABSTRACT: The facultative intracellular bacterium Listeria monocytogenes (Lm) may cause severe infection in humans and livestock. Control of acute listeriosis is primarily dependent on innate immune responses, which are strongly regulated by NF-κB, and tissue protective factors including fibrin. However, molecular pathways connecting NF-κB and fibrin production are poorly described. Here, we investigated whether the deubiquitinating enzyme CYLD, which is an inhibitor of NF-κB-dependent immune responses, regulated these protective host responses in murine listeriosis. Upon high dose systemic infection, all C57BL/6 Cyld(-/-) mice survived, whereas 100% of wildtype mice succumbed due to severe liver pathology with impaired pathogen control and hemorrhage within 6 days. Upon in vitro infection with Lm, CYLD reduced NF-κB-dependent production of reactive oxygen species, interleukin (IL)-6 secretion, and control of bacteria in macrophages. Furthermore, Western blot analyses showed that CYLD impaired STAT3-dependent fibrin production in cultivated hepatocytes. Immunoprecipitation experiments revealed that CYLD interacted with STAT3 in the cytoplasm and strongly reduced K63-ubiquitination of STAT3 in IL-6 stimulated hepatocytes. In addition, CYLD diminished IL-6-induced STAT3 activity by reducing nuclear accumulation of phosphorylated STAT3. In vivo, CYLD also reduced hepatic STAT3 K63-ubiquitination and activation, NF-κB activation, IL-6 and NOX2 mRNA production as well as fibrin production in murine listeriosis. In vivo neutralization of IL-6 by anti-IL-6 antibody, STAT3 by siRNA, and fibrin by warfarin treatment, respectively, demonstrated that IL-6-induced, STAT3-mediated fibrin production significantly contributed to protection in Cyld(-/-) mice. In addition, in vivo Cyld siRNA treatment increased STAT3 phosphorylation, fibrin production, pathogen control and survival of Lm-infected WT mice illustrating that therapeutic inhibition of CYLD augments the protective NF-κB/IL-6/STAT3 pathway and fibrin production.
    PLoS Pathogens 06/2013; 9(6):e1003455. · 8.14 Impact Factor
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    ABSTRACT: Primary lymphoma of the central nervous system (PCNSL) is defined as lymphoma of the diffuse large B-cell type confined to the CNS. To understand the effects of the CNS microenvironment on the malignant B cells and their interactions with the cells of the target organ, we analyzed a syngeneic mouse model. Transplantation of BAL17 cells into the frontal white matter of syngeneic BALB/c mice induced lymphomas with major clinical and neuropathologic features that parallel those of human PCNSL, including an angiocentric growth pattern in the brain parenchyma and tropism for the inner and outer ventricular system. Seven cycles of repeated isolation of lymphoma cells from the CNS and their intracerebral reimplantation induced genotypic and phenotypic alterations in resulting BAL17VII cells; the affected genes regulate apoptosis and are of the JAK/STAT pathway. Because lymphoma growth of BAL17VII cells was significantly accelerated, that is, shortening the time to death of the mice, these data indicate that prolonged stay of the lymphoma cells in the CNS was associated with worse outcome. These findings suggest that the CNS microenvironment fosters aggressiveness of lymphoma cells, thereby accelerating the lethal course of PCNSL.
    Journal of neuropathology and experimental neurology. 03/2013;
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    ABSTRACT: The differential diagnosis of lymphoid lesions in the central nervous system covers a broad spectrum of neoplastic and inflammatory disorders. Complex cases benefit from the combined expertise in the fields of hematopoietic and neuroepithelial tumors as well as neuroimmunology. The Network Lymphomas and Lymphomatoid Lesions in the Nervous System (NLLLN) recommends performing a biopsy prior to any therapeutic intervention as a precise diagnosis was impossible in approximately 50 % of patients pretreated with corticosteroids. This is based on the analysis of approximately 1,000 cases in the past 4 years. In addition to total NLLLN experiences the characteristics, pathogenesis and differential diagnosis of primary lymphoma of the central nervous system are discussed.
    Der Pathologe 03/2013; · 0.62 Impact Factor
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    ABSTRACT: AIM: The role of chemokines and their receptors, which regulate trafficking and homing of leukocytes to inflamed organs in human or murine autoimmune neuritis has not yet been elucidated in detail, Therefore, the role of the chemokine receptors CXCR4 and CXCR7 and their ligand CXCL12 was studied in autoimmune-mediated inflammation of the peripheral nervous system. METHODS: CXCL12/CXCR4- and/or CXCL12/CXCR7-interactions were specifically inhibited by the compounds AMD3100 or CCX771, respectively, in experimental autoimmune neuritis (EAN) of C57BL/6J mice immunized with P0106-125 peptide. RESULTS: Disease activity was significantly suppressed by blocking CXCR7 while antagonization of CXCR4 enhanced disease activity. Enhanced disease activity was accompanied by significantly increased transcription of IFN-γ, IL-12, and TNF-α mRNA in regional lymph nodes and spleen as well as by increased serum levels of IFN-γ. Furthermore, by blocking CXCR4, expression of the cell adhesion molecules ICAM-1 and VCAM-1 was upregulated on vascular endothelial cells of the sciatic nerve which coincided with significantly increased infiltration of the sciatic nerve by CD4+ T cells and macrophages. Remarkably, combined antagonization of both CXCR4 and CXCR7 significantly suppressed disease activity. This was accompanied by increased frequencies of activated and highly IFN-γ-expressing, P0106-125 -specific T cells in regional lymph nodes and spleen, however, these cells were unable to infiltrate the sciatic nerve. CONCLUSION: These data suggest differential and hierarchically ordered roles for CXCR4/CXCL12- versus CXCR7/CXCL12-dependent effects during EAN: CXCR7/CXCL12-interaction is a gatekeeper for pathogenic cells, regardless of their CXCR4/CXCL12-dependent state of activation.
    Neuropathology and Applied Neurobiology 03/2013; · 4.84 Impact Factor
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    ABSTRACT: Extramedullary plasmacytomas originating in the spinal cord are extremely rare lesions. We report a 52-year-old man presenting with progressive tetraparesis. Spinal magnetic resonance imaging (MRI) showed an ill-defined contrast-enhancing intramedullary mass at the C5-6 level. After a biopsy was taken, pathology including immunohistochemistry revealed plasmacytoma. Complete workup for multiple myeloma was negative. The patient was treated with intravenous chemotherapy followed by radiotherapy and corticosteroids without any improvement of the clinical symptoms or decreased tumor size on the follow-up MRIs. The most common spinal manifestation of plasmocytoma is involvement of the vertebral bodies leading to extradural compression of the cord. Only rarely plasmocytoma manifests itself as a primarily dural lesion leading to an intradural cord compression. This report describes the extremely rare manifestation of plasmocytoma of the spinal cord itself that therefore should be considered in the differential diagnosis of spinal cord mass lesions.
    Journal of neurological surgery. Part A, Central European neurosurgery. 12/2012;
  • Acta Neuropathologica 11/2012; · 9.73 Impact Factor
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    ABSTRACT: Abstract Background: Listeria monocytogenes usually causes mild maternal illness, but can be devastating to the fetus. Case: Listeriosis in a pregnant patient successfully treated with empiric antibiotic therapy is described. After induced delivery, despite severe placental infection, a healthy infant was born. Additionally, archived placental specimens with similar pathological manifestation were evaluated for evidence of L. monocytogenes. Conclusion: It is important to emphasize the value of associating maternal data and clinical and laboratory findings of the newborn with the pathologic placental findings to get better results in the etiologic diagnosis of the listeriosis.
    The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 10/2012; · 1.36 Impact Factor
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    ABSTRACT: In T-cell-mediated autoimmune diseases of the CNS, apoptosis of Fas(+) T cells by FasL contributes to resolution of disease. However, the apoptosis-inducing cell population still remains to be identified. To address the role of astrocytic FasL in the regulation of T-cell apoptosis in experimental autoimmune encephalomyelitis, we immunised C57BL/6 GFAP-Cre FasL(fl/fl) mice selectively lacking FasL in astrocytes with MOG(35-55) peptide. GFAP-Cre FasL(fl/fl) mice were unable to resolve EAE and suffered from persisting demyelination and paralysis, while FasL(fl/fl) control mice recovered. In contrast to FasL(fl/fl) mice, GFAP-Cre FasL(fl/fl) mice failed to induce apoptosis of Fas(+) activated CD4(+) T cells and to increase numbers of Foxp3(+) Treg cells beyond day 15 post immunisation, the time point of maximal clinical disease in control mice. The persistence of activated and GM-CSF-producing CD4(+) T cells in GFAP-Cre FasL(fl/fl) mice also resulted in an increased IL-17, IFN-γ, TNF and GM-CSF mRNA expression in the CNS. In vitro, FasL(+) but not FasL(-) astrocytes induced caspase-3 expression and apoptosis of activated T cells. In conclusion, FasL expression of astrocytes plays an important role in the control and elimination of autoimmune T cells from the CNS, thereby determining recovery from EAE.
    European Journal of Immunology 09/2012; · 4.97 Impact Factor
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    ABSTRACT: The roles of Toll-like receptors (TLRs) and their myeloid differentiation response gene 88 (MyD88)-dependent and MyD88-independent signaling cascade particularly with regard to the pathogenesis and regulation of immune responses in idiopathic inflammatory myopathies are unclear. We investigated these pathways in muscle biopsies from 5 cases each of polymyositis, inclusion body myositis, dermatomyositis, vasculitis-associated interstitial myositis, and noninflammatory neurogenic atrophy. Toll-like receptor 2, TLR4, TLR9, and MyD88 mRNA transcripts and protein expression were increased in all subtypes of idiopathic inflammatory myopathies. Upregulation of MyD88 was associated with increased mRNA levels of interferon-γ, interleukin 12p40, and interleukin 17, suggesting NF-κB activation via the MyD88-dependent pathway in early stages. The costimulatory molecules CD80 and CD86 were expressed on inflammatory infiltrates in idiopathic inflammatory myopathies and may additionally contribute to activation of the MyD88-independent pathway, leading to nuclear factor-κB activation in late stages. Our data suggest that nuclear factor-κB activation via both the MyD88-dependent and the MyD88-independent pathways contributes to the proinflammatory milieu in idiopathic inflammatory myopathies.
    Journal of Neuropathology and Experimental Neurology 09/2012; 71(10):855-67. · 4.35 Impact Factor
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    ABSTRACT: Myelin-specific CD8(+) T cells are thought to contribute to the pathogenesis of multiple sclerosis. Here we modeled this contribution in mice with CD8(+) T cells recognizing ovalbumin (OVA) expressed in oligodendrocytes (ODCs). Surprisingly, even very high numbers of activated OVA-reactive CD8(+) T cells failed to induce disease and were cleared from the immune system after antigen encounter in the central nervous system (CNS). Peripheral infection with OVA-expressing Listeria (Lm-OVA) enabled CD8(+) T cells to enter the CNS, leading to the deletion of OVA-specific clones after OVA recognition on ODCs. In contrast, intracerebral infection allowed OVA-reactive CD8(+) T cells to cause demyelinating disease. Thus, in response to infection, CD8(+) T cells also patrol the CNS. If the CNS itself is infected, they destroy ODCs upon cognate antigen recognition in pursuit of pathogen eradication. In the sterile brain, however, antigen recognition on ODCs results in their deletion, thereby maintaining tolerance.
    Immunity 06/2012; 37(1):134-46. · 19.80 Impact Factor
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    ABSTRACT: The obligate intracellular parasite Toxoplasma gondii infects and persists within neurons of approximately one-third of the human population. Intracerebral control of T. gondii largely depends on interferon (IFN)-γ-producing T cells, which induce antiparasitic effector mechanisms in infected cells, as well as immunosuppressive cytokines, which prevent immunopathology. To gain further insight into the role of neurons in Toxoplasma encephalitis (TE), we generated C57BL/6 synapsin-I (Syn)-Cre gp130(fl/fl) mice, which lack gp130, the signal-transducing receptor for the IL-6 family of cytokines, in their neurons. On infection with T. gondii, Syn-Cre gp130(fl/fl) mice failed to control T. gondii infection and died of necrotizing TE before day 77. In contrast, gp130(fl/fl) control mice efficiently restricted parasite replication and survived the infection. TE in Syn-Cre gp130(fl/fl) mice was characterized by a hyperinflammatory immune response with increased numbers of IL-17- and IFN-γ-producing CD4 and CD8 T cells but reduced intracerebral production of immunosuppressive transforming growth factor (TGF)-β and IL-27. Additional in vitro experiments found that IL-6 stimulation of neurons induced gp130-dependent TGF-β1, TGF-β2, and IL-27 production. Importantly, gp130 expression and stimulation with IL-6 cytokine family members also reduced death and apoptosis of infected cultured neurons. Correspondingly, TE in Syn-Cre gp130(fl/fl) but not gp130(fl/fl) mice was characterized by progressive neuronal loss. Collectively, these findings indicate a crucial protective function of gp130-expressing neurons in a model of chronic encephalitis.
    American Journal Of Pathology 05/2012; 181(1):163-73. · 4.52 Impact Factor
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    ABSTRACT: We evaluated the efficacy of interstitial brachytherapy (IBT) using (125)Iodine ((125)I) seeds for treatment of papillary tumors of the pineal region. Between September 2003 and September 2010, four patients (M/F = 2/2; median age, 57.3 years; range 29.2-69.1 years) with papillary tumors of the pineal region underwent IBT using (125)I seeds. Before brachytherapy two patients underwent endoscopic ventriculo-cisternotomy, because of occlusive hydrocephalus, and subsequent microsurgical resection was performed on one; three patients were primarily treated with IBT. Median tumor volume was 3.3 ml (range 1.6-4 ml), the tumor surface dose ranged between 50 and 65 Gy. For three patients the seeds were implanted permanently whereas one patient received temporary implants (28 days). The median follow-up time was 53.6 months (range 13-103.4 months). After brachytherapy, follow-up MR images revealed complete remission in one patient, partial remission in two, and stable disease in the remaining patient. Neurological status improved in all patients (reduced headache and nausea/vomiting for four patients; improvement of oculomotor dysfunction for two of three patients partially and for one of three patients completely). Neither treatment-related morbidity nor mortality was observed. Our results are indicative of good local control of papillary tumors of the pineal region after IBT, without treatment-related morbidity.
    Journal of Neuro-Oncology 04/2012; 109(1):99-104. · 3.12 Impact Factor
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    ABSTRACT: BACKGROUND: We evaluated the long-term outcome in patients harboring intracranial ependymomas treated with interstitial brachytherapy (IBT). METHODS: Twenty-one patients (M/F = 9/12; median age: 29 years; range: 8-70 years), diagnosed with intracranial ependymoma (1 WHO I, 11 WHO II, 9 WHO III) were treated with IBT using stereotactically implanted (125)Iodine seeds between 1987 and 2010, either primarily, as adjuvant therapy following incomplete resection, or as salvage treatment upon tumor recurrence. Sixteen of 21 patients underwent microsurgical resection prior to IBT; in 5 patients, IBT was performed primarily after stereotactic biopsy for histological diagnosis. The cumulative tumor surface dose ranged from 50-65 Gy treating a median tumor volume of 3.6 ml (range, 0.3-11.6 ml). A median follow-up period of 105.3 months (range, 12.7-286.2 months) was evaluated. RESULTS: Actuarial 2-, 5- and 10-years overall- and disease-specific survival rates after IBT were each 90% and 100% at all times for ependymomas WHO I/II, for anaplastic ependymomas WHO III 100%, 100%, 70% and 100%, 100%, 86%, respectively. The neurological status of seven patients improved, while there was no change in 12 and deterioration in 2 patients, respectively. Follow-up MR images disclosed a complete tumor remission in 3, a partial remission in 12 and a stable disease in 6 patients. Treatment-associated morbidity only occurred in a single patient. CONCLUSIONS: This study shows that stereotactic IBT for intracranial ependymomas is safe and can provide a high degree of local tumor control. Due to the low rate of side effects, IBT may evolve into an attractive alternative to microsurgery in ependymomas located in eloquent areas or as a salvage treatment.
    PLoS ONE 01/2012; 7(11):e47266. · 3.73 Impact Factor
  • Acta Neuropathologica 12/2011; 122(6):791-2. · 9.73 Impact Factor

Publication Stats

3k Citations
671.97 Total Impact Points


  • 2001–2014
    • University of Cologne
      • • Department of Neurology
      • • Department of Neuroradiology
      Köln, North Rhine-Westphalia, Germany
    • University of Bonn - Medical Center
      Bonn, North Rhine-Westphalia, Germany
    • Universitätsklinikum Freiburg
      • Department of Neurology and Neurophysiology
      Freiburg, Lower Saxony, Germany
  • 2013
    • Georg-August-Universität Göttingen
      Göttingen, Lower Saxony, Germany
  • 2006–2013
    • Otto-von-Guericke-Universität Magdeburg
      • Institut für Medizinische Mikrobiologie
      Magdeburg, Saxony-Anhalt, Germany
  • 2008–2010
    • Ruhr-Universität Bochum
      Bochum, North Rhine-Westphalia, Germany
  • 2002–2010
    • University of Rijeka
      • Faculty of Medicine
      Rijeka, Primorsko-Goranska Zupanija, Croatia
  • 2009
    • Max Planck Institute for Neurological Research
      Köln, North Rhine-Westphalia, Germany
    • Christian-Albrechts-Universität zu Kiel
      • Institute of Phytopathology
      Kiel, Schleswig-Holstein, Germany
  • 2000–2007
    • Universität Heidelberg
      • • Department of Parasitology
      • • Institute of Medical Microbiology and Hygiene
      Heidelberg, Baden-Wuerttemberg, Germany
  • 2005
    • University of Duisburg-Essen
      Essen, North Rhine-Westphalia, Germany
  • 2000–2005
    • University of Bonn
      • Department of Neurobiology
      Bonn, North Rhine-Westphalia, Germany