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272 results on '"Steinbach, J P"'

1. Patterns, predictors and prognostic relevance of high-grade hematotoxicity after temozolomide or temozolomide-lomustine in the CeTeG/NOA-09 trial

Author

Weller, J., Schäfer, N., Schaub, C., Tzaridis, T., Zeyen, T., Schneider, M., Potthoff, A. L., Giordano, F. A., Steinbach, J. P., Zeiner, P. S., Kowalski, T., Sabel, M., Hau, P., Krex, D., Grauer, O., Goldbrunner, R., Schnell, O., Tabatabai, G., Ringel, F., Schmidt-Graf, F., Brehmer, S., Tonn, J. C., Bullinger, L., Vajkoczy, P., Glas, M., Vatter, H., Herrlinger, U., and Seidel, C.

Published
2023
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2. Motional Quantum Error Correction

Author

Steinbach, J. and Twamley, J.

Subjects
Quantum Physics
Abstract

We examine the dynamics of a qubit stored in the motional degrees of freedom of an ultra-cold ion in an ion trap which is subject to the decoherence effects of a finite-temperature bath. We discover an encoding of the qubit, in two of the motional modes of the ion, which is stable against the occurrence of either none or one quantum jump. For the case of a zero-temperature bath we describe how to transfer only the information concerning the occurrence of quantum jumps and their types to a measuring apparatus, without affecting the ion's motional state significantly. We then describe how to generate a unitary restoration of the qubit given the jump information, through Raman processes generated by a series of laser pulses., Comment: 24 Pages, RevTex, also see http://www.thphys.may.ie/jtwamley/jtwamley.html Submitted to PRA. (CHANGED to two-column style)

Published
1998

3. An efficient scheme for the deterministic maximal entanglement of N trapped ions

Author

Steinbach, J. and Gerry, C. C.

Subjects
Quantum Physics
Abstract

We propose a method for generating maximally entangled states of N two-level trapped ions. The method is deterministic and independent of the number of ions in the trap. It involves a controlled-NOT acting simultaneously on all the ions through a dispersive interaction. We explore the potential application of our scheme for high precision frequency standards., Comment: 4 pages, no figures, submitted to PRL, under review, Revised Version: Incorporated referee comments

Published
1998
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4. Engineering two-mode interactions in ion traps

Author

Steinbach, J., Twamley, J., and Knight, P. L.

Subjects
Quantum Physics
Abstract

We describe how two vibrational degrees of freedom of a single trapped ion can be coupled through the action of suitably-chosen laser excitation. We concentrate on a two-dimensional ion trap with dissimilar vibrational frequencies in the x- and y-directions of motion, and derive from first principles a variety of quantized two-mode couplings, concentrating on a linear coupling which takes excitations from one mode to another. We demonstrate how this can result in a state rotation, in which it is possible to transfer the motional state of the ion from say the x-direction to the y-direction without prior knowledge of that motional state., Comment: 12 pages, 5 figures, to appear in PRA

Published
1997
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5. Dark pair coherent states of the motion of a trapped ion

Author

Gou, S. -C., Steinbach, J., and Knight, P. L.

Subjects
Quantum Physics
Abstract

We propose a scheme for generating vibrational pair coherent states of the motion of an ion in a two-dimensional trap. In our scheme, the trapped ion is excited bichromatically by three laser beams along different directions in the X-Y plane of the ion trap. We show that if the initial vibrational state is given by a two-mode Fock state, the final steady state, indicated by the extinction of the fluorescence emitted by the ion, is a pure state. The motional state of the ion in the equilibrium realizes that of the highly-correlated pair coherent state., Comment: 14 pages, 3 figures

Published
1996
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7. NDRG1 prognosticates the natural course of disease in WHO grade II glioma

Author

Blaes, J., Weiler, M., Sahm, F., Hentschel, B., Osswald, M., Czabanka, M., Thomé, C. M., Schliesser, M. G., Pusch, S., Luger, S., Winkler, F., Radbruch, A., Jugold, M., Simon, M., Steinbach, J. P., Schackert, G., Tatagiba, M., Westphal, M., Tonn, J. C., Gramatzki, D., Pietsch, T., Hartmann, C., Glimm, H., Vajkoczy, P., von Deimling, A., Platten, M., Weller, M., and Wick, W.

Published
2014
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9. OS05.9.A Short-term fasting in glioma patients - Analysis of diet diaries and metabolic parameters of the ERGO2 trial

Author

Voss, M, primary, Wenger, K J, additional, von Mettenheim, N, additional, Bojunga, J, additional, Vetter, M, additional, Diehl, B, additional, Gerlach, R, additional, Ronellenfitsch, M W, additional, Franz, K, additional, Harter, P N, additional, Hattingen, E, additional, Steinbach, J P, additional, Rödel, C, additional, and Rieger, J, additional

Published
2021
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11. OS12.6.A Combination therapy of CAR-NK-cells and anti-PD-1 results in high efficacy against advanced-stage glioblastoma in a syngeneic mouse model and induces protective anti-tumor immunity in vivo

Author

Strassheimer, F, primary, Strecker, M I, additional, Alekseeva, T, additional, Macas, J, additional, Demes, M C, additional, Mildenberger, I C, additional, Tonn, T, additional, Wild, P J, additional, Sevenich, L, additional, Reiss, Y, additional, Harter, P N, additional, Plate, K H, additional, Wels, W S, additional, Steinbach, J P, additional, and Burger, M C, additional

Published
2021
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19. AAV-mediated gene transfer of a checkpoint inhibitor in combination with HER2-targeted CAR-NK cells as experimental therapy for glioblastoma.

Author

Strecker, M. I., Wlotzka, K., Strassheimer, F., Roller, B., Ludmirski, G., König, S., Röder, J., Opitz, C., Alekseeva, T., Reul, J., Sevenich, L., Tonn, T., Wels, W. S., Steinbach, J. P., Buchholz, C. J., and Burger, M. C.

Subjects
GENETIC transformation, IMMUNE checkpoint inhibitors, CELLULAR therapy, GENETIC vectors, GLIOBLASTOMA multiforme, IPILIMUMAB
Abstract

Glioblastoma (GB) is the most common primary brain tumor, which is characterized by low immunogenicity of tumor cells and prevalent immunosuppression in the tumor microenvironment (TME). Targeted local combination immunotherapy is a promising strategy to overcome these obstacles. Here, we evaluated tumor-cell specific delivery of an anti-PD-1 immunoadhesin (aPD-1) via a targeted adeno-associated viral vector (AAV) as well as HER2-specific NK-92/5.28.z (anti-HER2.CAR/NK-92) cells as components for a combination immunotherapy. In co-culture experiments, target-activated anti-HER2. CAR/NK-92 cells modified surrounding tumor cells and bystander immune cells by triggering the release of inflammatory cytokines and upregulation of PD-L1. Tumor cell-specific delivery of aPD-1 was achieved by displaying a HER2-specific designed ankyrin repeat protein (DARPin) on the AAV surface. HER2-AAV mediated gene transfer into GB cells correlated with HER2 expression levels, without inducing anti-viral responses in transduced cells. Furthermore, AAV-transduction did not interfere with anti-HER2.CAR/NK-92 cell-mediated tumor cell lysis. After selective transduction of HER2+ cells, aPD-1 expression was detected at the mRNA and protein level. The aPD-1 immunoadhesin was secreted in a time-dependent manner, bound its target on PD-1-expressing cells and was able to re-activate T cells by efficiently disrupting the PD-1/PD-L1 axis. Moreover, high intratumoral and low systemic aPD-1 concentrations were achieved following local injection of HER2-AAV into orthotopic tumor grafts in vivo. aPD-1 was selectively produced in tumor tissue and could be detected up to 10 days after a single HER2-AAV injection. In subcutaneous GL261-HER2 and Tu2449-HER2 immunocompetent mouse models, administration of the combination therapy significantly prolonged survival, including complete tumor control in several animals in the GL261-HER2 model. In summary, local therapy with aPD-1 encoding HER2-AAVs in combination with anti-HER2.CAR/NK-92 cells may be a promising novel strategy for GB immunotherapy with the potential to enhance efficacy and reduce systemic side effects of immune-checkpoint inhibitors. [ABSTRACT FROM AUTHOR]

Published
2022
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24. P12.04 Synergistic effects of combination therapy of CAR-NK cells and anti-PD-1 antibody result in high efficacy against advanced stage orthotopic glioblastoma grafts in a syngeneic mouse model and induce protective anti-tumor immunity in vivo

Author

Strassheimer, F, primary, Strecker, M I, additional, Zhang, C, additional, Mildenberger, I C, additional, Harter, P N, additional, Tonn, T, additional, Steinbach, J P, additional, Wels, W S, additional, and Burger, M C, additional

Published
2019
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25. OS6.5 ERGO2: A prospective randomized trial of a 9-day schedule of calorically restricted ketogenic diet and fasting or standard diet in addition to re-irradiation for malignant glioma

Author

Voss, M, primary, Wagner, M, additional, von Mettenheim, N, additional, Harter, P N, additional, Wenger, K, additional, Franz, K, additional, Bojunga, J, additional, Gerlach, R, additional, Glatzel, M, additional, Paulsen, F, additional, Hattingen, E, additional, Baehr, O, additional, Ronellenfitsch, M W, additional, Fokas, E, additional, Imhoff, D, additional, Steinbach, J P, additional, Rödel, C, additional, and Rieger, J, additional

Published
2019
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31. OS2.1 Objective responses to chemotherapy in recurrent glioma do not predict better survival: A prospective analysis from the German Glioma Network

Author

Bähr, O, primary, Hentschel, B, additional, Hattingen, E, additional, Reusche, M, additional, Tatagiba, M, additional, Tonn, J, additional, Schnell, O, additional, Schackert, G, additional, Westphal, M, additional, Herrlinger, U, additional, Pietsch, T, additional, Reifenberger, G, additional, Weller, M, additional, Löffler, M, additional, and Steinbach, J P, additional

Published
2018
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33. P07.01 The CAR2BRAIN study: a monocentric phase I trial with ErbB2-specific NK-92/5.28.z cells in recurrent glioblastoma

Author

Burger, M. C., Mildenberger, I. C., Cieplik, H. C., Zhang, C., Jennewein, L., Ihrig, K., Wagner, M., Mittelbronn, M., Senft, C., Tonn, T., Wels, W. S., and Steinbach, J. P.

Subjects
Cancer Research, Oncology, Neurology (clinical), POSTER PRESENTATIONS
Abstract

Natural killer cells (NK cells) are increasingly explored for adoptive cancer immunotherapy. Like T cells, NK cells can be genetically modified to express chimeric antigen receptors (CARs) that recognize tumor-associated cell surface antigens and mediate selective recognition and specific lysis of cancer cells, thereby overcoming endogenous resistance mechanisms in tumor cells. In two previous phase I clinical trials, the continuously expanding human NK cell line NK-92 has been safely applied as an allogeneic cell therapeutic with clinical responses observed in some of the cancer patients treated. To enhance efficiency and specificity, the ErbB2-specific cell clone NK-92/5.28.z was generated, which carries a codon-optimized CAR (CAR 5.28.z) based on ErbB2-specific antibody FRP5 and CD28 and CD3ζ signaling domains. Elevated ErbB2 (HER2) protein levels have been reported in a significant proportion of GBM tumors and were correlated with impaired survival. In preclinical studies, we could demonstrate high and specific activity of NK-92/5.28.z cells against established and primary ErbB2-positive glioblastoma cells. In orthotopic xenograft models in ­immunodeficient mice ­repetitive intracranial injections of NK-92/5.28.z cells led to a highly extended symptom-free survival. In an immunocompetent mouse model, repetitive intratumoral NK-92/5.28.z injections induced an endogenous immune response against syngeneic GL261/ErbB2 glioblastomas. This resulted in tumor rejection and long-term protection against tumor rechallenge. Based on these promising data, we designed the CAR2BRAIN trial (EudraCT number 2016-00025-39), a monocentric phase I dose finding trial investigating the safety and tolerability of NK-92/5.28.z cells as an allogeneic cell therapeutic in patients with recurrent glioblastoma. The NK-92/5.28.z cells will be injected during relapse surgery into the resection wall (dose escalation cohort; 9–18 patients), and in a second patient group repetitively through a Rickham reservoir into the resection cavity (expansion cohort; 6 patients). In the dose escalation part of the trial the highest cell number which can be applied safely will be established (maximum tolerated dose = MTD) with a maximum dose of up to 1x10^8 cells planned. After determination of the MTD in the dose escalation cohort, in addition to the initial injection into the resection wall up to twelve further injections through the Rickham reservoir will be carried out to establish safety of prolonged treatment in the expansion cohort. Distribution of the injected NK-92/5.28.z cells in the brain, the cerebrospinal fluid and the blood will be monitored. Furthermore, the immune reaction triggered against the target antigen ErbB2 as well as ErbB2-independent immune reactions will be characterized.

Published
2017

37. P03.21 Casp9 germline mutation in a family with multiple brain tumors

Author

Ronellenfitsch, M. W., primary, Oh, J., additional, Satomi, K., additional, Sumi, K., additional, Harter, P. N., additional, Steinbach, J. P., additional, Felsberg, J., additional, Capper, D., additional, Voegele, C., additional, Schittenhelm, J., additional, Mittelbronn, M., additional, and Ohgaki, H., additional

Published
2017
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38. ERGO: A pilot study of ketogenic diet in recurrent glioblastoma / Erratum

Author

Rieger, J, Bähr, O, Maurer, G D, Hattingen, E, Franz, K, Brucker, D, Walenta, S, Kämmerer, U, Coy, J F, Weller, M, Steinbach, J P, University of Zurich, and Rieger, J

Subjects
610 Medicine & health, 2730 Oncology, 1306 Cancer Research, 10040 Clinic for Neurology
Published
2014

45. MGMT Promoter Methylation Is a Strong Prognostic Biomarker for Benefit from Dose-Intensified Temozolomide Rechallenge in Progressive Glioblastoma: The DIRECTOR Trial

Author

Weller, Michael, Tabatabai, G, Kästner, B, Felsberg, J, Steinbach, J P, Wick, A, Schnell, O, Hau, P, Herrlinger, U, Sabel, M C, Wirsching, H G, Ketter, R, Bähr, O, Platten, M, Tonn, J C, Schlegel, U, Marosi, C, Goldbrunner, R, Stupp, R, Homicsko, K, Pichler, J, Nikkhah, G, Meixensberger, J, Vajkoczy, P, Kollias, S, Hüsing, J, Reifenberger, G, Wick, W, Weller, Michael, Tabatabai, G, Kästner, B, Felsberg, J, Steinbach, J P, Wick, A, Schnell, O, Hau, P, Herrlinger, U, Sabel, M C, Wirsching, H G, Ketter, R, Bähr, O, Platten, M, Tonn, J C, Schlegel, U, Marosi, C, Goldbrunner, R, Stupp, R, Homicsko, K, Pichler, J, Nikkhah, G, Meixensberger, J, Vajkoczy, P, Kollias, S, Hüsing, J, Reifenberger, G, and Wick, W

Abstract

PURPOSE Rechallenge with temozolomide (TMZ) at first progression of glioblastoma after temozolomide chemoradiotherapy (TMZ/RT→TMZ) has been studied in retrospective and single-arm prospective studies, applying temozolomide continuously or using 7/14 or 21/28 days schedules. The DIRECTOR trial sought to show superiority of the 7/14 regimen. PATIENTS AND METHODS Patients with glioblastoma at first progression after TMZ/RT→TMZ and at least two maintenance temozolomide cycles were randomized to Arm A [one week on (120 mg/m(2) per day)/one week off] or Arm B [3 weeks on (80 mg/m(2) per day)/one week off]. The primary endpoint was median time-to-treatment failure (TTF) defined as progression, premature temozolomide discontinuation for toxicity, or death from any cause. O(6)-methylguanine DNA methyltransferase (MGMT) promoter methylation was prospectively assessed by methylation-specific PCR. RESULTS Because of withdrawal of support, the trial was prematurely closed to accrual after 105 patients. There was a similar outcome in both arms for median TTF [A: 1.8 months; 95% confidence intervals (CI), 1.8-3.2 vs. B: 2.0 months; 95% CI, 1.8-3.5] and overall survival [A: 9.8 months (95% CI, 6.7-13.0) vs. B: 10.6 months (95% CI, 8.1-11.6)]. Median TTF in patients with MGMT-methylated tumors was 3.2 months (95% CI, 1.8-7.4) versus 1.8 months (95% CI, 1.8-2) in MGMT-unmethylated glioblastoma. Progression-free survival rates at 6 months (PFS-6) were 39.7% with versus 6.9% without MGMT promoter methylation. CONCLUSIONS Temozolomide rechallenge is a treatment option for MGMT promoter-methylated recurrent glioblastoma. Alternative strategies need to be considered for patients with progressive glioblastoma without MGMT promoter methylation. Clin Cancer Res; 1-8. ©2015 AACR.

Published
2015

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