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Molecular Neurooncology

Three to five of 100.000 people are annually diagnosed with a glioblastoma (GBM), the most malignant brain tumor in adults. Despite aggressive multimodal treatment including surgical resection and radiochemotherapy, the median survival time is only 12 to 15 months after diagnosis. The high malignancy of GBM is ascribed to its resistance towards chemotherapy and its invasive growth into the surrounding brain tissue, which explain the ineffectiveness of surgery and radiation. GBM-recurrence often arises from the spreading of tumor cells far away from their original occurrence. To date, there is no defined treatment standard in case of disease progression during or after standard therapy. Recurrent GBM limits life expectancy to only a few weeks. The research group “Molecular Neurooncology” concentrates on projects regarding GBM biology as well as to develop new therapeutic strategies to treat this tumor.

The research projects are funded by the German Cancer Research Foundation, Foundation Ulrike Sauer (ISUS), Software AG Foundation, Interdisciplinary Center for Clinical Research Tübingen, Henriette and Otmar-Eier-Foundation and the Else-Übelmesser-Foundation .

Research projects
Staff
Publications
Collaborations, partners and links

GLIOMA CELL PROGRESSION IS ASSOCIATED TO MOTILITY

The tumor suppressor gene p53, the “guardian of the genome”, is mutated in nearly 50 % of all tumors. p53 loss of function mutations are an important step in tumorigenesis and play a pivotal role in the development of cell death resistance, therefore also in the development of resistance towards chemotherapeutic drugs or irradiation. The restauration of p53 activity in glioma cells was suggested to be a promising approach for cancer gene therapy. The chimeric tumor suppressor 1 (CTS-1) is an artificial protein based on the structure and sequence of p53, but in contrast to p53, CTS-1 will not be inactivated or destroyed via proteasomal degradation, in this regard CTS-1 could also be named “dominant-positive p53”. CTS-1 induces cell death both in p53 mutant and p53 wildtype glioma cells. To identify new genes involved in the development of cell death resistance, we generated CTS-1resistant glioma cells and performed a whole genome expression analysis in CTS-1sensitive versus CTS-1resistant sibling cells. Approximately 1000 genes were differentially expressed. Many of these genes are involved in tumor associated processes such as migration, proliferation or apoptosis. In our analyses we found that the expression of many of these differentially expressed genes is regulated by NFκB. In addition, the CTS-1 dependent cell death was dependent on NFκB activity. In this context, we also analyzed the function of IκBζ, an untypical member of the inhibitor of NFκB” (IκB) family, a protein that was highly upregulated in CTS-1 resistant cells and that is suggested to regulate NFκB activity. We demonstrated that in glioma cells, IκBζ expression is induced by irradiation and upregulates the secretion of inflammatory cytokines by these cells. Overexpression of IκBζ in glioma specimen is correlated worse prognosis of glioma patients. Together with our collaboration partner Prof. Mittelbronn in Luxembourg we identified “Carboxypepidase E” (CPE) as a gene that is differentially expressed in CTS-1 resistant versus sensitive glioma cells. A secreted version of CPE provides anti-migratory, but pro-proliferative effects in glioma cells and is suggested to be a so called “switch factor” involved in the decision of a glioma cell either to stay and to proliferate or to migrate and to invade the healthy brain, if the living conditions in the tumor micro-milieu are suboptimal. CPE modulate the expression of EMT proteins in glioma cells, this way mitigating cell migration. Additionally, CPE regulates the metabolic switch toward glycolysis the tumor cell induces to escape starvation. Since glycolysis is associated to tumor cell motility, by this mechanism CPE also inhibits cell motility.

Naumann, U., Kügler, S., Wolburg, H., Wick, W., Rascher, G., Schulz, J.B., Conseiller, E., Bähr, M., Weller, M. Chimeric tumor suppressor 1 (CTS1), a p53-derived chimeric tumor suppressor gene, kills p53 mutant and p53 wild-type glioma cells in synergy with irradiation and CD95 ligand. Cancer Res. 61 (2001): 5833-5842

Naumann, U., Huang, H., Wolburg, H., Wischhusen, J., Weit, S., Ohgaki, H., Weller, M. PCTAIRE3 and PIG3: potential mediators of glioma cell death by CTS-1, a dominant-positive p53-derived tumor suppressor. Cancer Gene Ther. (2006) 13:469-478

Seznec, J., Weit, S., Naumann, U. Gene expression profile in a glioma cell line resistant to cell death induced by the chimeric tumorsuppressor-1 (CTS-1), a dominant positive p53 – the role of NFkB. Carcinogenesis (2010) 3:411-418

Seznec, J., Naumann, U. Microarray Analysis in a Cell Death Resistant Glioma Cell Line to Identify Signaling Pathways and Novel Genes Controlling Resistance and Malignancy. Cancers (2011) 3:2827-2843

Höring, E., Harter, P. N., Seznec, J., Schittenhelm, J., Bühring, H.J., Bhattacharyya, S., von Hattingen, E., Zachskorn, C., Mittelbronn, M., Naumann, U. The "go or grow" potential of gliomas is linked to the neuropeptide processing enzyme carboxypeptidase E and mediated by metabolic stress. Acta Neuropathol. (2012) 124:83-97

Brennenstuhl. H., Armento, A., Braczynski, A.K., Mittelbronn, M., Naumann, U. In glioma cells, IκBζ, an atypical member of the inhibitor of nuclear factor kappa B (NFkB) family, is induced by gamma irradiation, regulates cytokine expression and is associated with bad prognosis. Int. J. Oncol. (2015) 47:1971-1980

Ilina, E.I., Armento, A., Garea Sanchez, L., Reichlmeir, M., Braun, Y., Penski C., Capper, D., Sahm, F., Jennewein, L., Harter, P.N., Zukunft, S., Fleming, I., Schulte, D., Le Guerroué, F., Behrends, C., Ronellenfitsch, M.W., Naumann, U., Mittelbronn, M. Effects of soluble CPE on glioma cell migration are associated with mTOR activation and enhanced glucose flux, Oncotarget. 2017 Jun 27. doi: 10.18632/oncotarget.18747

Armento, A., Ilina, E.I., Kaoma, T., Muller, A., Vallar, L., Niclou, S.P., Krüger, MA., Mittelbronn, M. Naumann, U. Carboxypeptidase E transmits its anti-migratory function in glioma cells via transcriptional regulation of cell architecture and motility regulating factors. Int. J. Oncol. 2017, 51: 702-714, (DOI: 10.3892/ijo.2017.4051)

Granting:German Cancer Foundation, Interdisciplinary Center for Clinical Research Tübingen
(Prof. Dr. U. Naumann)  

THERAPEUTIC AND FUNCTIONAL EFFECTS OF VISCUMINS IN GLIOBLASTOMA 

Suppression of cellular immune responses is a common process in GBM and is one reason why this tumor is so malignant. Secretion of TGF-β is typical for glioma and correlates with the progression of glioma. TGF-β plays a key role in glioma mediated immunosuppression: it inhibits the activation of immune cells via downregulation of immune-activating ligands such as major histocompatibility complex, MHC class I polypeptide-related sequence-A and -B or of the UL16 binding proteins 1, -2 and -3. Additionally, TGF-β augments the differentiation from naïve into regulatory T cells, blocks the maturation of certain immune cells and induces cell death in Natural Killer (NK) and T cells. It has been known for long time that mistletoe lectins can stimulate immune effector cells such as macrophages, NK cells, as well as B and T lymphocytes. One effect of mistletoe lectin is the ability to induce the expression of pro-inflammatory interleukins and interferon γ in immune cells and to reduce TGF-ß secretion in glioma cells. Treatment of GBM cells with mistletoe preparations containing high concentrations of mistletoe lectin or with recombinant mistletoe lectin enhanced the immune cell mediated killing of GBM cells whereas preparations with low mistletoe lectin content did not. Besides this, mistletoe lectins provide anti-migratory capacity, block the expression of tumor-associated genes and, at higher concentration, induce cell death in tumor cells.

Podlech, O., Harter, P.N., Mittelbronn, M., Pöschel, S., Naumann, U. Fermented mistletoe extract as a multimodal antitumoral agent in gliomas. Evid Based Complement Alternat Med. (2012):501796. doi: 10.1155/2012/501796.

Schötterl, S., Naumann, U. Mistletoe compounds as anticancer drugs: Effects and mechanisms in the treatment of Glioblastoma. Translational Research in Biomedicine: Mistletoe: From Mythology to Evidence-Based Medicine, Karger Press, 2015; Vol. 4:48-57

Schötterl, S., Hübner, M., Armento, A., Veninga, V., Wirsik, N.M., Bernatz, S., Lentzen, H., Mittelbronn, M., Naumann, U. Viscumins functionally modulate cell motility associated gene expression. Int. J. Oncol. 2017; 50: 684-696

Schötterl, S., Mittelbronn, M., Lentzen, H., Naumann, U. Effects of mistletoe lectins on the natural killer (NK) cell activity against glioma cells. Die Mistel in der Tumortherapie IV, KVC-Verlag Essen 2016,149-160

Granting: Foundation Ulrike Sauer (ISUS), Software AG Foundation, Förderverein komplementärmedizinische Forschung Arlesheim, Switzerland (Prof. Dr. U. Naumann)

ONCOLYTIC VIRUSES TO TREAT GBM 

Oncolytic virotherapy is upcoming discipline in cancer research. Oncolytic viruses are natural or genetically modified viruses that are able to eliminate malignant cancer cells, leaving non-neoplastic cells unharmed. Oncolytic viruses have been shown to be safe in patients in many clinical trials. In our studies we analyzed the therapeutic effects of Ad-Delo3-RGD in experimental glioma. The replication of this virus is dependent on YB-1, a factor highly upregulated in chemotherapy resistant glioma cells and in recurrent glioma. In collaboration with PD Dr. Holm in Munich we could demonstrate that Ad-Delo3-RGD selectively replicates in YB-1positive glioma cells, but not in non-cancerous astrocytes, kills chemotherapy resistant GBM cells with stem cell properties and, in an experimental mouse glioma model, significantly increases the survival of tumor-bearing animals. A clinical trial using this virus as a therapeutic agent for the treatment of recurrent glioma will start end of 2016 in Frankfurt/Main. In a collaborative study with Prof. Per Sonne Holm in Munich we are now interested if glioma standard therapy such as tumor irradiation as well as immunotherapeutic strategies can potentiate the therapeutic effect of Ad-Delo3-RGD.

Mantwill, K, Naumann, U., Seznec, J., Girbinger, V., Lage, H. Surowiak P., Beier, C., Mittelbronn, M., Schlegel, J, Holm, P.S. 2013. YB-1 dependent oncolytic adenovirus efficiently inhibits tumor growth of glioma cancer stem like cells. Translational Med. 2013, 11:216

Naumann, U., Holm, P.S. Oncovirotherapy of glioblastoma – a kind of immunotherapy? Brain Disorders and Therapy( 2015), dx.doi.org/10.4172/2168-975X.S2-001


Granting: BMBF (Holm), Else-Übermesser-Stiftung (Naumann), German Research Foundation (Holm, Naumann)

 

THE FUNCTION OF PERICYTES IN GBM NEOANGIOGENESIS 

A key hallmark of GBM is the generation of new blood vessels that are on the one hand a central diagnostic feature and on the other hand a current target for treatment strategies. One pathological hallmark that distinguishes GBM from lower grade glioma is its abundant and aberrant vasculature. The malformed GBM vasculature is accompanied by vessel permeability and the breakdown of the blood-brain barrier (BBB). We recently identified that pericytes are the major cell type of newly formed blood vessels within glioblastoma, the so-called vascular proliferations. The formation of those vascular proliferations is poorly understood to date, however we provided first evidence that especially epithelial-to-mesenchymal transcription factors (EMT) such as Slug and Twist are selectively upregulated in pericytes/vessel-associated mural cells when new blood vessels are generated. Therefore, it is essential to understand the underlying mechanisms of how glioma cells modulate EMT factors in pericytes during glioma-associated angiogenesis and the related functional consequences in pericytes regarding their involvement formation of malformed tumor vessel and loss of the BBB.

Mäder, L., Blank, A.E., Capper, D., Jangsong, J., Baumgarten, P., Wirsik, N.M., Penski, C., Ehlers, J., Seifert, M., Klink, B., Liebner, S., Niclou, S., Naumann, U., , Harter, P.N., Mittelbronn, M. Pericytes/vessel-associated mural cells (VAMCs) are the major source of key epithelial-mesenchymal transition (EMT) factors SLUG and TWIST in human glioma, Oncotarget, 2018 (in press)

Granting: Interdisciplinary Center for Clinical Research Tübingen,


 
Name
Department
Phone
Email
 Abdullah Alekuzei
Abdullah Alekuzei Medical Student
Molecular Neuro-Oncology
 
 Jacob Ehlers
Jacob Ehlers Medical Student
Molecular Neuro-Oncology
 
Prof. Dr. Ulrike Naumann
Prof. Dr. Ulrike Naumann Research Group Leader
Molecular Neuro-Oncology
07071 29-80707 
 Yana Parfyonova
Yana Parfyonova
Molecular Neuro-Oncology
15238832586 
 NIKHIL RANJAN
NIKHIL RANJAN
Molecular Neuro-Oncology
 
 Sonja Schoetterl
Sonja Schoetterl PhD Student
Molecular Neuro-Oncology
07071 29-80707 
medical student Leonie Schumacher
medical student Leonie Schumacher
Molecular Neuro-Oncology
 

 

2018

Mäder, L., Blank, A.E., Capper, D., Jangsong, J., Baumgarten, P., Wirsik, N.M., Penski, C., Ehlers, J., Seifert, M., Klink, B., Liebner, S., Niclou, S., Naumann, U., , Harter, P.N., Mittelbronn, M. Pericytes/vessel-associated mural cells (VAMCs) are the major source of key epithelial-mesenchymal transition (EMT) factors SLUG and TWIST in human glioma, Oncotarget, 2018 (in press)

2017

Schötterl, S., Hübner, M., Armento, A., Veninga, V., Wirsik, N.M., Bernatz, S., Lentzen, H., Mittelbronn, M., Naumann, U. Viscumins functionally modulate cell motility associated gene expression. Int. J. Oncol. 2017; 50:  684-696

Armento, A., Ilina, E.I., Kaoma, T., Muller, A., Vallar, L., Niclou, S.P., Krüger, MA., Mittelbronn, M. Naumann, U. Carboxypeptidase E transmits its anti-migratory function in glioma cells via transcriptional regulation of cell architecture and motility regulating factors. Int. J. Oncol. 2017, 51: 702-714, (DOI: 10.3892/ijo.2017.4051)

Ilina, E.I., Armento, A., Garea Sanchez, L., Reichlmeir, M., Braun, Y., Penski C., Capper, D., Sahm, F., Jennewein, L., Harter, P.N., Zukunft, S., Fleming, I., Schulte, D., Le Guerroué, F., Behrends, C., Ronellenfitsch, M.W., Naumann, U., Mittelbronn, M. Effects of soluble CPE on glioma cell migration are associated with mTOR activation and enhanced glucose flux, Oncotarget. 2017 Jun 27. doi: 10.18632/oncotarget.18747

2016

Schötterl, S., Mittelbronn, M., Lentzen, H., Naumann, U. Effects of mistletoe lectins on the natural killer (NK) cell activity against glioma cells. Die Mistel in der Tumortherapie IV, KVC-Verlag Essen 2016,149-160

Dhayade, S., Kaesler, S., Sinnberg, T., Dobrowinski, H., Peters, S., Naumann, U., Liu, H., Hunger, R.R., Thunemann, M., Biedermann, T., Schittek, B., Simon, H.U., Feil, S., Feil, R. A Novel Melanoma-Promoting cGMP Pathway that is Potentiated by Sildenafil. Cell Reports (2016) in press

2015

Brennenstuhl, H., Armento, A., Braczysnki, A. K., Mittelbronn, M., Naumann, U. In glioma cells, IkBζ, an atypical member of the inhibitor of nuclear factor kappa B (NFB) family, is induced by gamma irradiation, regulates cytokine secretion and is associated with bad prognosis. Int. J. Oncol. 47, 2015: 1971-1980 (DOI: 10.3892/ijo.2015.3159)

Kumar, P., Naumann, U., Aigner, L., Wischhusen, J., Beier, C.P., Beier, D. Impaired TGF- induced growth inhibition contributes to the increased proliferation rate of neural stem cells harboring mutant p53. Am. J. Cancer Res. 2015;5(11):3436-3445

Schötterl, S., Brennenstuhl, H., Naumann U. Modulation of Immune Responses by Histone Deacetylase Inhibitors. Critical Reviews in Oncogenesis 2015, 20(1–2):139–154

Schötterl, S., Naumann, U. Mistletoe compounds as anticancer drugs: Effects and mechanisms in the treatment of Glioblastoma. Translational Research in Biomedicine: Mistletoe: From Mythology to Evidence-Based Medicine, Karger Press, 2015; Vol. 4:48-57

Naumann, U., Holm, P.S. Oncovirotherapy of glioblastoma – a kind of immunotherapy? Brain Disorders and Therapy 2015, http://dx.doi.org/10.4172/2168-975X.S2-001

2014


Höring, E., Podlech, O., Silkenstedt, B., Rota, I.A., Naumann, U "The histone deacetylase inhibitor trichostatin a promotes apoptosis and antitumor immunity in glioblastoma cells". World Biomedical Frontiers (ISSN: 2328-0166) 2014. http://biomedfrontiers.org/cancer-2014-4-29/

2013

Naumann, U. Harter, P.N., Rubel, J., Ilina, E., Blank, A.E., Esteban, H.B., Mittelbronn, M. (2013).Glioma cell migration and invasion as potential target for novel treatment strategies. Translational Neuroscience  4(3): 314-329

Mantwill K1, Naumann U,Seznec J, Girbinger V, Lage H, Surowiak P, Beier D, Mittelbronn M, Schlegel J, Holm PS.  YB-1 dependent oncolytic adenovirus efficiently inhibits tumor growth of glioma cancer stem like cells. J Transl Med. 2013;11:216.

Noell, S., Feigl, G.C., Serifi, D., Mayer, D., Naumann, U., Göbel, W., Ehrhardt, A. Ritz, R. Microendoscopy for hypericin fluorescence tumor diagnosis in a subcutaneous glioma mouse model. Photodiagn Photodyn 2013 (in press)

Adamopoulou, E., Naumann, U. (2013). HDAC inhibitors and their potential application in human glioblastoma treatment.  Onco Immunol 2(8): eLocation ID: e25219

Höring, E., Podlech, O., Silkenstedt, B., Rota, I.A., Naumann, U. The Histone Deacetylase Inhibitor Trichostatin A Promotes Apoptosis and Antitumor Immunity in Glioblastoma Cells. Anticancer Res 2013,33(4):1351-1360

Naumann, U. Harter, P.N., Rubel, J., Ilina, E., Blank, A.E., Esteban, H.B., Mittelbronn, M. (2013).Glioma cell migration and invasion as potential target for novel treatment strategies. Translational Neuroscience  4(3): 314-329

Mantwill K1, Naumann U,Seznec J, Girbinger V, Lage H, Surowiak P, Beier D, Mittelbronn M, Schlegel J, Holm PS.  YB-1 dependent oncolytic adenovirus efficiently inhibits tumor growth of glioma cancer stem like cells. J Transl Med. 2013;11:216.

Noell, S., Feigl, G.C., Serifi, D., Mayer, D., Naumann, U., Göbel, W., Ehrhardt, A. Ritz, R. Microendoscopy for hypericin fluorescence tumor diagnosis in a subcutaneous glioma mouse model. Photodiagn Photodyn 2013 (in press)

Adamopoulou, E., Naumann, U. (2013). HDAC inhibitors and their potential application in human glioblastoma treatment.  Onco Immunol 2(8): eLocation ID: e25219

Höring, E., Podlech, O., Silkenstedt, B., Rota, I.A., Naumann, U. The Histone Deacetylase Inhibitor Trichostatin A Promotes Apoptosis and Antitumor Immunity in Glioblastoma Cells. Anticancer Res 2013,33(4):1351-1360 

2012


Podlech, O., Harter, P.N., Mittelbronn, M., Pöschel, S., Naumann, U. Fermented mistletoe extract as a multimodal antitumoral agent in gliomas. Evid Bases Complement Alternat Med. 2012;2012:501796. doi: 10.1155/2012/501796.

Höring, E., Harter, P.N., Seznec, J., Schittenhelm, J., Bühring, H.J., Bhattacharyya, S., Hattingen, E., Zachskorn, C., Mittelbronn, M., Naumann, U. The “go or grow” potential of gliomas is linked to the neuropeptide processing enzyme carboxypeptidase E and mediated by metabolic stress. Acta Neuropathologica, Epub ahead 

2011

Seznec, J., Silkenstedt, B., Naumann, U. Therapeutic effects of the Sp1 inhibitor mithramycin A in glioblastoma J Neurooncol. (2011) 101(3):365-377

Gaub, P., Yoshi, Y., Wuttke, A,. Naumann, U., Schnichels, S., Heiduschka, P., Di Giovanni, S. The histone acetyltransferase p300 promotes intrinsic axonal regeneration. Brain (2011)  134:2134-2148

Seznec, J., Naumann, U. Microarray Analysis in a Cell Death Resistant Glioma Cell Line to Identify Signaling Pathways and Novel Genes Controlling Resistance and Malignancy. Cancers 2011 3:2827-2843

2010

Seznec, J., Weit, S., Naumann, U. Gene expression profile in a glioma cell line resistant to cell death induced by the chimeric tumorsuppressor-1 (CTS-1), a dominant positive p53 – the role of NFkB
Carcinogenesis (2010) 3:411-418

2009

Tedeschi, A., Nguyen, T., Steele, S.U., Feil, S., Feil, R., Naumann, U. , Di Giovanni, S. The tumour suppressor p53 regulates cGKI expression during neuronal maturation and is required for cGMP-dependent growth cone collapse. J. Neuro Sci. (in press)

Naumann, U., Weller, M. Modulating TGF-ß receptor signaling: a novel approach of cancer therapy. In Transforming Growth Factor-beta in Cancer Therapy, published in Beverly Teicher's Methods in Molecular Biology series on "Cancer Drug Discovery and Development" (Humana Press, USA 2009)

2008 

Weinmann, L., Wischhusen, J., Demma, M.J., Naumann, U., Roth, P., DasMahapatra, B., Weller, M. A novel p53 rescue compound induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis. Cell Death Differ. (2008) 15:718-729

Naumann, U., Maass, P., Gleske, A.K., Aulwurm, S., Weller, M., Eisele, G. Glioma gene therapy with soluble transforming growth factor-ß receptors II and III. Int J. Oncol. (2008) 33:759-765

2007

Naumann, U., Bähr, O., Wolburg, H., Altenberend, S., Wick, W., Liston, P., Ashkenazi, A., and Weller, M. Adenoviral expression of XIAP antisense RNA induces apoptosis in glioma cells and suppresses the growth of xenografts in nude mice. Gene Ther. (2007) 14:147-161; 14:1434-1437

2006

Weiler, M., Bähr, O., Hohlweg,U., Naumann, U., Rieger, J., Huang, H., Tabatabai, G., Ohgaki, H., Weller,M., Wick, W. BCL-xL, apoptosis and motility: move to survive or survive to move? Cell Death Differ. (2006) 13:1156-1169

Busche, A., Goldmann, T., Naumann, U., Steinle, A. Brandau, S. Natural killer cell-mediated rejection of experimental human lung cancer by genetic overexpression of major histocompatibility complex class I chain-related gene; A. Hum. Gene Ther. 17 (2006): 135-146

Naumann, U., Huang, H., Wolburg, H., Wischhusen, J., Weit, S., Ohgaki, H., Weller, M. PCTAIRE3 and PIG3: potential mediators of glioma cell death by CTS-1, a dominant-positive p53-derived tumor suppressor. Cancer Gene Ther. (2006) 13:469-478

Wick, W., Naumann, U., und Weller, M. (2006). Transforming growth factor-beta: a molecular target for the future therapy of glioblastoma. Current pharmaceutical design 12, 341-349 

Hirrlinger PG, Scheller A, Braun C, Hirrlinger J, Kirchhoff F. Temporal control of gene recombination in astrocytes by transgenic expression of the tamoxifen-inducible DNA recombinase variant CreERT2.
Glia. 2006 Jul;54(1):11-20

2005

Amatya, V.J., Naumann, U., Weller, M., Ohgaki, O.TP53 promoter methylation in human gliomas;Acta Neuropathologica 110 (2005): 178-184 

Hirrlinger PG, Scheller A, Braun C, Quintela-Schneider M, Fuss B, Hirrlinger J, Kirchhoff F.Expression of reef coral fluorescent proteins in the central nervous system of transgenic mice.
Mol. Cell Neurosci. 2005 Nov;30(3):291-303

2004

Naumann, U., Wick, W., Beschorner, R., Meyermann, R., Weller, M. Expression and functional activity of osteoprotegerin in human malignant glioma. Acta Neuropathol. 107 (2004):17-22

Naumann, U., Wick, W., Beschorner, R., Meyermann, R., Weller, M. Reply to Lorenz et al.: Osteoprotegerin in the central nervous system. Acta Neuropathol. 107 (2004): 578

Herrlinger, U., Aulwurm, S., Strik, H., Weit, S., Naumann, U., Weller, M. MIP-1alpha antagonizes the effect of a GM-CSF-enhanced subcutaneous vaccine in a mouse glioma model.
J. Neurooncol. 66 (2004): 147-154 

Naumann, U., Wischhusen, J., Weit, S., Rieger, J., Wolburg, H., Massing. U., Weller, M. Alkyphosphocholine-induced glioma cell death is BCL-XL-sensitive, caspase-independent and characterized by massive cytoplasmic vacuole formation.
Cell Death and Differ. 11 (2004): 1326-1341

Biglari, A., Bataille, D., Naumann, U., Weller, M., Castro, M.G., Lowenstein, P.R. Effects of ectopic decorin in modulating intracranial glioma progress in vivo, a rat syngeneic model.
Cancer Gene Ther. 11 (2004):721-732

2003

Naumann, U., Waltereit, R., Schulz, J.B., Weller, M. Adenoviral (full length) Apo2L/TRAIL gene transfer is an ineffective treatment strategy for malignant glioma.
J. Neuro-Oncology 61 (2003): 7-15

Naumann, U., Schmidt, F., Wick, W., Frank, B., Weit, S., Gilllissen, B., Daniel, P., Weller, M. Adenoviral natural born gene therapy for malignant glioma.
Human Gene Ther. 14 (2003): 1235-1246

Platten, M., Kretz, A., Naumann, U., Aulwurm, S., Egashira, K., Isenmann, S., Weller M. Monocyte chemoattractant protein-1 increases microglial infiltration and aggressiveness of gliomas.
Ann. Neurol. 54 (2003): 388-392

Wischhusen, J., Naumann, U., Ohgaki, H., Rastinejad, F., Weller, M. CP-31398, a novel p53-stabilizing agent, induces p53-dependent and p53-independent cell death.
Oncogene 22 (2003): 8233-8145 

Friese, M.A., Platten, M., Lutz, S.Z., Naumann, U., Aulwurm, S., Bischof, F., Bühring, H.J., Dichgans, J., Rammensee, H.G., Steinle, A., Weller, M. MICA/NKG2D-mediated immunogene therapy of experimental gliomas. Cancer Res. 63 (2003) : 8996-9006.

2001

Roth, W., Wagenknecht, B., Klumpp, A., Naumann, U., Hahne, M., Tschopp, J., Weller, M. APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis.
Cell Death and Diff. 8 (2001): 403-410

Streffer, J.R., Rimner, A., Rieger, J., Naumann, U., Rodemann, H.P., and Weller, M. Bcl-2 family protein expression modulates radiosensitivity in human glioma cells.
J. Neuro-Oncol. 56 (2001) : 43-49

Schmidt, F., Rieger, J., Wischhusen, J., Naumann, U., Weller, M. Glioma cell sensitivity to topotecan: the role of p53 and topotecan-induced DNA damage.
Eur. J. Pharmacol. 412 (2001): 21-25

Weber, R.G., Rieger, J., Naumann, U., Lichter, P., Weller, M. Chromosomal imbalances associated with the response to chemotherapy and cytotoxic cytokines in human malignant glioma cell lines.
Int. J. Cancer 91 (2001): 213-218

Rimner, A., Wischhusen, J., Naumann, U., Gleichmann, M., Steinbach, J.P., Weller, M. Identification by suppression subtractive hybridization of p21 as a radio-inducible gene in human glioma cells.
Anticancer Res. 21 (2001): 3505-3508

Leitlein, J., Aulwurm, S., Waltereit, R., Naumann, U., Wagenknecht, B., Garten, W., Weller, M., Platten. M. Processing of immunosuppressive pro-TGF-beta 1, 2 by human glioblastoma cells involves cytoplasmic and secreted furin-like proteases.
J.Immunol. 166 (2001): 7238-7243

Röhn, T.A., Wagenknecht, B., Roth, W., Naumann, U., Gulbins, E., Krammer, P.H., Walczak, H., Weller, M. CCNU-dependent potentiation of TRAIL/Apo2L-induced apoptosis in human glioma cells is p53-independent but may involve enhanced cytochrome c release
Oncogene 20 (2001): 4128-4137

Naumann, U., Kügler, S., Wolburg, H., Wick, W., Rascher, G., Schulz, J.B., Conseiller, E., Bähr, M., Weller, M. Chimeric tumor suppressor 1 (CTS1), a p53-derived chimeric tumor suppressor gene, kills p53 mutant and p53 wild-type glioma cells in synergy with irradiation and CD95 ligand.
Cancer Res. 61 (2001): 5833-5842

Naumann, U., Weit, S., Wischhusen, J., Weller, M. Diva/Boo is a negative regulator of cell death in human glioma cells.FEBS Let. 505 (2001): 23-26

2000

Vietor, M., Winter, S., Groscurth, P., Naumann, U., Weller, M. On the significance of telomerase activity in human malignant glioma cells.
Eur. J. Pharmacol. 407 (2000): 27-37 

1999 

Roller, A., Bähr, O.R., Streffer, J., Winter, S., Heneka, M., Deininger, M., Meyermann, R., Naumann, U., Gulbins, E., Weller, M. Selective potentation of drug cytotoxicity by NSAID in human glioma cells: The role of COX-1 and MRP. Biochem. Biophys. Res. Comm. 259 (1999): 600-605 

Pohl, U., Wagenknecht, B., Naumann, U., Weller, M. p53 enhances BAK and CD95 expression in human malignant glioma cells but does not enhance CD95L-induced apoptosis.
Cell. Physiol. Biochem. 9 (1999): 29-37

Roth, W., Isenmann, S., Naumann, U., Kügler, S., Bähr, M., Dichgans, J., Ashkenazi, A., Weller, M. Locoregional Apo2L/TRAIL eradicates intracranial human malignant glioma xenografts in athymic mice in absence of neurotoxicity. Biochem. Biophys. Res. Comm. 265 (1999): 479-483 

Wagenknecht, B., Glaser, T., Naumann, U., Kügler, S., Isenmann, S., Bähr, M., Korneluk, M., Liston, P., Weller, M. Expression and biological activity of X-linked inhibitor of apoptosis (XIAP) in human malignant glioma.
Cell Death and Diff. 6 (1999): 370-376 

Wick, W., Furnari, F.B., Naumann, U., Cavanee, W.K., Weller, M. PTEN gene transfer in human malignant glioma: sensitization to irradiation and CD95L-induced apoptosis.
Oncogene 18 (1999): 3936-3943 

Bartussek, C., Naumann, U., Weller, M. Accumulation of p53 modulates the growth, clonogenicity and radiochemosensitivity of malignant glioma cells independently of their endogenous p53 status.
Exp. Cell. Res. 253 (1999): 432-439 

Münz, C., Naumann, U., Grimmel, C., Rammensee, H.G., Weller, M. TGF-beta-independent induction of immunogenicity by decorin gene tansfer in human malignant glioma cells.
Eur. J. Immunol. 29 (1999): 1032-1040 

Naumann, U., Weit, S., Rieger, L., Meyermann, R., Weller, M. p27 modulates cell cycle progression and chemosensitivity in human malignant glioma.
Biochem. Biophys. Res. Comm. 261 (1999): 890-896 

Ständer, M., Naumann, U., Wick, W., Weller, M. Transforming growth factor-beta and p21: multiple molecular targets of decorin-mediated suppression of neoplastic growth.
Cell Tissue Res. 296 (1999): 221-227

1998 

Rieger, J., Naumann, U., Glaser, T., Ashkenazi, A., Weller, M. Apo2 ligand: a novel lethal weapon against malignant glioma?
FEBS letters 427 (1998): 124-148 

Ständer, M., Naumann, U., Dumitrescu, L., Heneka, M., Löschmann, P., Gulbins, E., Dichgans, J.,
Weller, M. Decorin gene transfer-mediated suppression of TGF-ß synthesis abrogates experimental malignant glioma growth in vivo.
Gene Therapy 5 (1998): 1187-1194

Naumann, U., Weller, M. Retroviral Bax gene tranfer fails to sensitize malignant glioma cells to CD95L-induced apoptosis and cancer chemotheraapy.
Int. J. Cancer 77 (1998): 1-4 

Naumann, U., Durka, S., Weller, M. Dexamethasone-mediated protection from drug cytotoxicity: association with p21WAF1/CIP1 protein accumulation?
Oncogene 17 (1998): 1567-75

1996

Naumann, U., Eisenmann-Tappe, I, Rapp, U.R: Role of Raf kinases in development and growth of tumorsRec. Res. Canc. Res. 143 (1996): 237-244

 

 

 

Sascha Venturelli, Physiology, UKT Tübingen

Lusine Danielyan, Pharmacology, University of Tübingen

Michel Mittelbronn, Neuropathologie, Edinger  Institut, Goethe Universität, Frankfurt a.M.

Per Sonne Holm, Experimentelle Tumortherapie, Urologie, Klinikum Rechts der Isar, TU München

Bernd Pichler, Institut für Präklinische Bildgebung und Radiopharmazie, Universität Tübingen

Robert Feil, Signaltransduktion, Transgene Modell, IFIB, Tübingen

Simone Niclou, Neuroonkologie, Norlux, CRP Sante, Luxemburg

Partick Müller, Friedrich-Miescher-Laboratorium, MPG, Tübingen

Karin Schilbach, Hämatologie, Kinderklinik, UKT Tübingen

Stephan Huber, Radioonkologie, UKT Tübingen

XVir Therapeutics GmbH, München

Melema Pharma GmbH, Köln 

ISCADOR AG ,Lörrach, www.iscador.com/de/ 

 

NOA: Neuroonkologische Arbeitsgemeinschaft (NOA ) in der Deutschen Krebsgesellschaft

ZNO: Zentrum für Neuroonkologie (ZNO)

Deutsches Gliomnetzwerk

EORTC

BMBF: http://www.bmbf.de/

Deutsche Krebshilfe: http://www.krebshilfe.de

Software AG Stiftung: www.sagst.de/

Innovationsstiftung Sauer: www.isus-stiftung.de/

Research group leader
Prof. Ulrike Naumann ulrike.naumannuni-tuebingen.de Address

Center of Neurology
Hertie Institute for Clinical Brain Research
Department Neurology and Stroke

Otfried-Müller-Straße 27
72076 Tübingen

Phone: +49 (0)7071 29-80707
Fax: +49 (0)7071 29-25150