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328 results on '"Erttmann, R."'

1. Bone Marrow Transplantation from Mismatched Unrelated Donors

Author

Zander, A. R., Zabelina, T., Löliger, C., Krüger, W., Eiermann, T., Renges, H., Dürren, M., Finckenstein, F., Kabisch, H., Erttmann, R., Kröger, N., Berdel, W. E., editor, Büchner, Th., editor, Kienast, J., editor, Jürgens, H., editor, Ritter, J., editor, and Vormoor, J., editor

Published
2003
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2. Stem Cell Transplantation in Acute Myeloid Leukemia after Conditioning with Busulfan, Cyclophosphamide and Different Dosages of Etoposide (VP-16)

Author

Kröger, N., Zabelina, T., Sonnenberg, S., Krüger, W., Renges, H., Stute, N., Finkenstein, F., Mayer, U., Holstein, K., Fiedler, W., Colberg, H., Sonnen, R., Kuse, R., Braumann, D., Metzner, B., del Valle, F., Erttmann, R., Kabisch, H., Zander, A. R., Berdel, W. E., editor, Büchner, Th., editor, Kienast, J., editor, Jürgens, H., editor, Ritter, J., editor, and Vormoor, J., editor

Published
2003
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10. Scientific Proceedings Second International Symposium on Cytostatic Drug Resistance

Author

Hill, Bridget T., Hosking, L. K., McClean, S., Shellard, S. A., Dempke, W. C. M., Whelan, R. D. H., Sehested, M., Friche, E., Demant, E. J. F., Jensen, P. B., Kopnin, B. P., Wolf, B., Seidel, A., Nickelsen, M., Brandt, I., Heinemann, G., Dietel, M., Bremer, S., Hoof, T., Tümmler, B., Broxterman, H. J., Versantvoort, C. H. M., Kuiper, C. M., Feller, N., Schuurhuis, G. J., Lankelma, J., Gupta, S., Tsuruo, T., Kim, C., Gollapudi, S., Bittl, A., Nap, M., Jäger, W., Lathan, B., Lang, N., Raikhlin, N. T., Perevozchikov, A. G., Volodina, J. L., Licht T., Fiebig H. H., Bross K. J., Herrmann F., Mertelsmann R., Bashir, I., Sikora, K., Foster, C. S., Castagna, M., Viacava, P., Cianfrigliao, M., Favati, A., Collecchi, P., Caligo, M. A., Cipollini, G., Bevilacqua, G., Schrenk, D., Gant, T. W., Silverman, J. A., Thorgeirsson, S. S., Harstrick, A., Zhang, Z. G., Schmoll, H. J., Rustum, Y., Mitze, M., Beck, T., Weikel, W., Brumm, C., Knapstein, P. G., McDonald, T., Gardner, P., Kang, N., van der Heyden, S. A. M., Elst, H. J., Stein, U., Jandrig, B., Krause, H., Schmidt-Peter, P., Frege, J., Wunderlich, V., Boven, E., van Kalken, C. K., Pinedo, H. M., Gebauer, W., Fallgren-Gebauer, E., Diete, M., Wagner, T., Müller, M. R., Lennartz, K., Nowrousian, H. R., Seeber, S., Shtil, A. A., Kazarov, A. R., Gudkov, A. V., Stavrovskaya, A. A., Djuraeva, F. H., Stromskaya, T. P., Noller, A., Frese, G., Neumann, M., Wilisch, A., Probst, H., Gekeler, V., Handgretinger, R., Schmidt, H., Muller, C. P., Dopfer, R., Klingebiel, T., Niethammer, D., Weger, S., Diddens, H., Daumiller, E., Bunge, A., Lilischkis, R., Salmassi, A., Kopun M., Scherthan H., Granzow C., Leuschner, I., Schmidt, D., Hoffmann, H., Harms, D., Scagliotli, G. V., Leonardo, E., Cappia, S., Esposito, G., Tombesi, M., Cianfriglia, M., Esposito, G. V., Merendino, N., Viora, M., Caserta, M., Tritarelli, E., Rocca, E., Boccoli, G., Samoggia, P., Fossati, C., Testa, U., Peschle, C., Darling, J. L., Ashmore, S. M., Peterson, D. C., Thomas, D. G. T., Kramer, R. A., Stanlunas, R., Summerhayes, T., Lion, T., Shoemaker, R. H., Wu, L., Smythe, A., Boyd, M. R., Beck, W. T., Danks, M. K., Wolverton, J. S., Chen, M., Bugg, B. Y., Suttle, D. P., Catapano, C. V., Fernandes, D. J., Gieseler, F., Boege, F., Erttmann, R., Arps, H., Zwelling, L., Wilms, K., Biersack, H., Kaspers, G. J. L., Pieters, R., Klumper, E., de Waal, F. C., van Wering, E. R., Veerman, A. J. P., Schmidt, C. A., Lorenz, F., Schäfer, A., Kirsch, A., Siegert, W., Huhn, D., Simon, W. E., Siebert, G., Schneider, M., Oettling, M., Reymann, A., Entmann, R., Schmidt, S., Woermann, C., Windmeier, C., Herzig, I., Schaefer, B., Heidebrecht, H. J., Wacker, H. H., Künnemann, H., van Heijningen, Th. H. M., Slovak, M. L., Baak, J. P. A., Steidtmann, K., Fichtinger-Schepman, A. -M. J., Hill, B. I., Scanlon, K. J., Zeller, W. J., Chen, G., Gietema, J. A., de Vries, E. G. E, Sleijfer, D.Th, Willemse, P. H. B., Guchelaar, H. J., Uges, D. R. A., Aulenbacher, P., Voegeli, R., Mulder, N. H., Skrezek, C., Bertermann, H., Eichholtz-Wirth, H., Born, R., Bier, H., Koch, M., Bernhardt, G., Hählen, K., Reile, H., van Zantwijk, C. H., Wering, E. R. van, Görögh, T., Lippert, B., Werner, J. A., Eickbohm, J. E., Mickiseh, G. H., Gottesman, M. M., Pastan, I., Hofmann, J., Wolf, A., Spitaler, M., Bock, G., Grunicke, H., Ponstingl, H., Roth, I., Granzow, C., Dörner, C., Erttmann, R., Looft, G., Ossenkoppele, G. J., Scheffer, G. L., Atassi, G., Pierre, A., Kraus, L., Leonce, S., Regnier, G., Dhainaut, A., Ponstingl H., Stöhr M., Rohlff, C., Glazer, R. I., Cho-Chung, Y. S., Höllt, V., Kouba, M., Vogt, G., Allmeier, H., Nissen, N. I., Cros, S., Guilbaud, N., Dunn, T., Berlion, M., Atassi, G., Bizzari, J. P., Messing, A. M., Matuschek, A., Mutter, I., Kiwit, J. C. W., Bastian, L., Goretzki, P. E., Frilling, A., Simon, D., Röher, H. D., Reichle, A., Altmayr, F., Rastetter, J., Erbil, C., Jaques, G., Maasberg, M., Havemann, K., Häußermann, K., Heidebrecht, H. -J., Van de Vrie, W., Gheuens, E. E. O., Durante, N. M. C., De Bruijn, E. A., Marquet, R. L., Van Oosterom, A. T., Eggermont, A. M. M., Stow, M. W., Vickers, S. E., Warr, J. R., Roller, E., Eichelbaum, M., Klumpp, B., Krause, J., Schumacher, K., Hörner, S., Laßmann, A., Traugott, U., Schlick, E., Bürkle, D., Futscher BW, List AF, Dalton WS, Ladda, E., Bühl, K., Weimer, A., Eser, C., Hamprecht, K., Schalk, K. P., Jackisch, C., Brandt, B., Blum, M., Louwen, F., Schulz, K., Hanker, J. P., Rüther, U., Schmidt, A., Müller, H. A. G., Nunnensiek, C., Bader, H., Eisenberger, F., Jipp, P., Niethammer, B., Muller, C., Ling, V., Joncourt, F., Redmond, S., Stöhr, M., Buser, K., Fey, M., Tobler, A., Brunner, K., Gratwohl, A., Cerrry, T., Nuessler, V., Pelka-Fleischer, R., Nerl, C., Beckert, B., Wilmanns, W., Hegewisch-Becker, S., Fliegner, M., Zander, A., Hossfeld, D. K., Blanz, J., Mewes, K., Ehninger, G., Zeller, K. -P., Schuldes, H., Herrmann, G., Boeckmann, W., Schroeder, R., Jonas, D., Zurborn, K. -H., Bruhn, H. D., Uharek, L., Glass, B., Gassmann, W., Loeffler, H., Mueller-Ruohholtz, W., Gassmann W., Glass B., Uharek L., Loeffler H., Mueller-Ruchholtz W., Jaquet, K., Kreipe, H., Felgner, J., Radzun, H. J., Parwaresch, M. R., Kogan EA, Mazurenko NN, Sekamova SM, Wolf, H., Röhe, K., Wilkens, K., Clausen, M., Henze, E., van der Bosch, J., Rüller, S., Schlaak, M., Köhl, U., Schwabe, D., Rohrbach, E., Montag, E., Bauer, S., Cinatl, J., Cinatl, Jr, I., Mainke, M., Geiss, H., Kornhuber, B., Juhl, H., Stritzel, H., Kalhoff, H., Schniegel, W., Menke, T., Pröbsting, B., Schulze-Westhoff, P., Boos, J., Weidner, J., Wedemeyer, N., Wiedorn, K., Ueda, Y., Blasius, S., Wuisman, P., Böcker, W., Roessner, A., Dockhorn-Dworniczak, B., Ramm, D., Knebel, J., Sass, W., Aufderheide, M., and Seifert, J.

Published
1991
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28. Effect of intraarterial versus intravenous cisplatin in addition to systemic doxorubicin, high-dose methotrexate, and ifosfamide on histologic tumor response in osteosarcoma (Study COSS-86)

Author

Winkler, K., Bielack, S., Delling, G., Salzer-Kuntschik, M., Kotz, R., Greenshaw, C., Jurgens, H., Ritter, J., Kusnierz-Glaz, C., Erttmann, R., Gadicke, G., Graf, N., Ladenstein, R., Leyvraz, S., Mertens, R., and Weinel, P.

Subjects
Cisplatin -- Health aspects, Osteosarcoma, Injections, Intra-arterial -- Evaluation, Bone cancer, Cisplatin -- Dosage and administration, Health
Abstract

Local treatment of bone cancer produced survival rates on the order of 15 to 20 percent. Newer methods of aggressive chemotherapy have improved this outcome dramatically; rates of survival, free from metastasis, range from 60 to 70 percent. These rates are sufficiently good that it becomes important to consider the quality of life afforded by the treatment, which, in the case of bone cancer, usually refers to the preservation of a limb. There is some theoretical advantage to the use of an intraarterial injection for chemotherapy for bone cancer. If the cancer is in, for example, the leg, then an injection into the appropriate artery will carry the chemotherapeutic agent directly towards the tumor. On the other hand, an intravenous injection will carry the agent first to the heart, from which it will be spread equally throughout the body. The intraarterial injection may also have an advantage in that the venous return from the limb can be restricted by a tourniquet, thus giving tissue in the limb greater time to absorb the chemotherapeutic agent from the blood. However, while these conceptual notions may seem appealing, any true benefit must be demonstrated experimentally. While intraarterial injections have been reported to be effective, a previously published direct comparison of intraarterial and intravenous injection failed to demonstrate a beneficial effect for intraarterial injection. This study, however, involved several different drug regimens that were not directly comparable. In the current study patients were given high-dose methotrexate, doxorubicin, and ifosfamide intravenously; in addition, each patient also received cisplatin either intraarterially or intravenously. No significant differences in response were observed between the intravenous and the intraarterial groups, indicating that the intraarterial injection does not provide appreciable benefit in this aggressive chemotherapy scheme. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

31. Adjuvant chemotherapy in osteosarcoma — Effects of cisplatinum, BCD, and fibroblast interferon in sequential combination with HD-MTX and adriamycin: Preliminary results of the COSS 80 study

Author

Winkler, K., Beron, G., Kotz, R., Salzer-Kuntschik, M., Beck, J., Beck, W., Brandeis, W., Ebell, W., Erttmann, R., Göbel, U., Havers, W., Henze, G., Hinderfeld, L., Höcker, P., Jobke, A., Jürgens, H., Kabisch, H., Landbeck, G., Preusser, P., Prindull, G., Ramach, W., Ritter, J., Sekera, J., Treuner, J., and Wüst, G.

Published
1983
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40. Human natural immunoglobulin M antibodies induce apoptosis of human neuroblastoma cells by binding to a Mr 260,000 antigen

Author

David K, Markus W. Ollert, Vollmert C, Heiligtag S, Eickhoff B, Erttmann R, Bredehorst R, and Cw, Vogel

Subjects
Male, Skin Neoplasms, Immunoglobulins, Apoptosis, Bone Neoplasms, DNA Fragmentation, Mice, Neuroblastoma, Rats, Nude, Antibody Specificity, Antigens, Neoplasm, Rhabdomyosarcoma, Tumor Cells, Cultured, Animals, Humans, Melanoma, Osteosarcoma, Goats, Immunization, Passive, Flow Cytometry, Rats, Molecular Weight, Immunoglobulin M, Immunoglobulin G, Chickens, Neoplasm Transplantation
Abstract

Sera of healthy humans contain natural cytotoxic IgM antibodies that specifically recognize a Mr 260,000 antigen (NB-p260) on the surface of human neuroblastoma (NB) cells. Here we demonstrate that anti-NB IgM antibodies prepared from different healthy individuals induce, in all human NB cell lines analyzed thus far, typical morphological and biochemical features of apoptosis including nuclear fragmentation, chromatin condensation, and DNA fragmentation. Both the binding of human anti-NB IgM to NB cells and the induction of apoptosis could be inhibited by preincubation of NB cells with murine IgG raised against purified NB-p260. Furthermore, preincubation of human anti-NB IgM with purified NB-p260 immobilized onto a solid support abolished its ability to induce apoptosis in NB cells. Natural human anti-NB IgM failed to bind to and induce apoptosis in control tumor cell lines that lack expression of NB-p260. The anti-NB IgM-induced apoptotic response was also observed in vivo in xenografted human NB tumors. After a single i.v. injection of anti-NB IgM into nude rats bearing solid NB xenografts, many areas of pyknotic cells with fragmented nuclei were observed that stained positive using the terminal dUTP nick end labeling method. In conclusion, the data demonstrate that natural anti-NB IgM antibodies in the sera of healthy individuals are potent mediators of apoptotic cell death of NB cells both in vitro and in vivo. The NB-p260 antigen was identified as the apoptosis-inducing receptor for anti-NB IgM. Whereas natural anti-NB IgM and NB-p260 may be useful tools for immunotherapy of NB, their biological significance remains to be determined.

Published
1999

41. T-cell mediated suppression of neuroblastoma following fractalkine gene therapy is amplified by targeted IL-2

Author

Lode, H., Erttmann, R., Xiang, R., Zeng, Yan, Lode, H., Erttmann, R., Xiang, R., and Zeng, Yan

Abstract

Das Induzieren und Aufrechterhalten einer tumor-protektiven Immunität sind wesentliche Ziele in der Immuntherapie des Neuroblastoms. Eine Erhöhung der Anzahl von tumor-infiltrierenden Leukozyten könnte ein Weg sein, um dieses Ziel zu erreichen. Fractalkine ist ein besonderes TH1 CX3C Chemokin, welches sowohl Adhäsion und Migration von Leukozyten vermittelt. Gerichtetes IL-2 (ch14.18-IL-2) wurde durch eine genetische Fusion von anti-GD2 Antikörper mit IL-2 hergestellt, damit IL-2 spezifisch in das Mikromilieu von Neuroblastomen gebracht werden kann. In dieser Arbeit habe ich die Hypothese getestet, dass Gentherapie mit dem Chemokin Fractalkine (FKN) eine wirksame Antineuroblastom-Immunantwort induziert, welche durch gerichtetes IL-2 amplifiziert wird. Zu diesem Zweck wurden NXS2-Zellen genetisch verändert, damit sie murines FKN produzieren (NXS2-FKN). Transkription und Expression des mFKN Gens konnte in NXS2-FKN Zellen und Tumorgewebe gezeigt werden. Die chemotaktische Eigenschaft von FKN wurde sowohl in vitro als auch in vivo gezeigt. FKN zeigte eine Reduktion des Primärtumorwachstums, welches durch gerichtetes IL-2 mit nicht-kurativen Dosen von ch14.18-IL-2 deutlich verbessert wurde. Ferner wurden experimentelle Lebermetastasen nur in den Mäusen komplett eradiziert, welche die Kombinationstherapie erhalten haben. Die Mechanismen, welche an dieser Antitumorantwort beteiligt sind, schließen eine wirksame T-Zell-Aktivierung (Hochregulation von CD69, CD25, und von TNF-alpha und INF-gamma), sowie eine Erhöhung der tumorspezifischen CTL-Aktivität mitein. Die Depletion von CD4+ und CD8+ T-Zellen in vivo hat diesen therapeutischen Effekt aufgehoben, was die essentielle Rolle von T-Zellen in diesem immuntherapeutischen Ansatz unterstreicht. Zusammenfassend konnte ich zum ersten Mal zeigen, dass Chemokin-Gentherapie mit FKN durch gerichtetes IL-2 amplifiziert wird, was eine Kombination dieser beiden Strategien zur adjuvanten Therapie beim Neuroblastom nahe legt., Induction and maintenance of tumor-protective immunity are the major goals of neuroblastoma immunotherapy. Enhancing the amount of tumor infiltrating leukocytes might be a way to achieve these goals since they may be associated with residual evidence of the ineffective immune response. Fractalkine is a unique TH1 CX3C chemokine known to induce both adhesion and migration of leukocytes mediated by a membrane-bound and a soluble form, respectively. Targeted IL-2 (ch14.18-IL-2) was constructed by anti-GD2 antibody fused with IL-2 so that IL-2 can be directed into the microenvironment of neuroblastoma tumor. Here, I tested the hypothesis that chemokine gene therapy with fractalkine (FKN) induces an effective anti-neuroblastoma immune response amplified by targeted IL-2. NXS2 cells were engineered to stably produce murine FKN (NXS2-FKN). Transcrip- tion and expression of the mFKN gene in NXS2-FKN cells and tumor tissue were demonstrated. The chemotactic activity of FKN expressed by NXS2 cells was determined both in vitro and in vivo. Importantly, NXS2-FKN exhibited a reduction in primary tumor growth, which was boosted by targeted IL-2 using non-curative doses of ch14.18-IL-2. Furthermore, experimental liver metastases were completely eradicated in mice receiving the combination therapy, demonstrating the induction of a long-lived tumor protective response. The mechanisms involved in antitumor response included effective T cell activation as indicated by the up-regulation of T-cell activation markers (CD69, CD25) and proinflammatory cytokines (TNF-alpha, INF-gamma) as well as the enhancement of tumor specific CTL activity. The depletion of CD4+ and CD8+ T cells in vivo abrogated the therapeutic effect supporting the crucial role of T cells in this immunotherapeutic approach. In summary, I demonstrated for the first time that chemokine gene therapy with FKN is amplified by targeted IL-2 suggesting a combination of both strategies as an adjuvant therapy for neuroblastoma.

Published
2006

42. Comparison of the diagnostic and prognostic value of biological markers in neuroblastoma. Proposal for a common methodology of analysis. SENSE group

Author

Favrot, M. C., Ambros, P., Schilling, F., Frappaz, D., Combaret, V., Berthold, F., Dominici, Carlo, Erttmann, R., Esteve, J., Jenkner, A., Kerbl, R., Mann, J., Mathieu, P., Parker, L., Powell, J., and Philip, T.

Subjects
Neuroblastoma, Child, Preschool, Biomarkers, Tumor, Humans, Infant, Prognosis
Abstract

The prognosis of pediatric neuroblastoma depends both on clinical presentation and on certain cellular and molecular characteristics. Screening programs have been initiated in infants of less than one year of age, based on the hypothesis that neuroblastoma progresses from early to late clinical stages through a classical multistep process linked to an accumulation of molecular abnormalities. However, recent analyses suggest that most cases discovered by screening are low stage tumors considered as dysembryogenetic residues devoid from major abnormalities and that high-grade tumors with molecular abnormalities are unrelated diseases.To confirm one or the other hypothesis, and eventually identify biological factors possibly responsible for the initiation and progression of the disease, it is of utmost importance that all investigators agree on biological criteria for analysis when neuroblastoma tissue is available in screened and unscreened populations. This paper reviews the biological tools available for prognosis in neuroblastoma, the priority for analysis of biological markers according to both methodological reliability and feasibility, and the conditions of tissue storage for further analysis of these biological markers.The standardized biological evaluation of neuroblastoma will allow to collect sufficient data for multivariate analysis; such analysis is now fundamental if one wants to clearly define the respective impacts of biological abnormalities on neuroblastoma progression.

Published
1996

44. Einfluß des lokalchirurgischen Vorgehens auf die Inzidenz von Metastasen nach neoadjuvanter Chemotherapie des Osteosarkoms

Author

Winkler, K., primary, Beron, G., additional, Kotz, R., additional, Salzer-Kuntschik, M., additional, Beck, J., additional, Beck, W., additional, Brandeis, W., additional, Ebell, W., additional, Erttmann, R., additional, Göbel, U., additional, Havers, W., additional, Henze, G., additional, Hinderfeld, L., additional, Höcker, P., additional, Jobke, A., additional, Jürgens, H., additional, Kabisch, H., additional, Preusser, P., additional, Prindull, G., additional, Ramach, W., additional, Ritter, J., additional, Sekera, J., additional, Treuner, J., additional, and Wüst, G., additional

Published
2008
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45. Comparable results in patients with acute lymphoblastic leukemia after related and unrelated stem cell transplantation

Author

Dahlke, J, primary, Kröger, N, additional, Zabelina, T, additional, Ayuk, F, additional, Fehse, N, additional, Wolschke, C, additional, Waschke, O, additional, Schieder, H, additional, Renges, H, additional, Krüger, W, additional, Kruell, A, additional, Hinke, A, additional, Erttmann, R, additional, Kabisch, H, additional, and Zander, A R, additional

Published
2005
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