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8 results on '"Kriege, Oliver"'

1. Real-World Experience of CPX-351 As First-Line Treatment in 188 Patients with Acute Myeloid Leukemia

Author

Rautenberg, Christina, primary, Stölzel, Friedrich, additional, Röllig, Christoph, additional, Stelljes, Matthias, additional, Gaidzik, Verena I, additional, Lauseker, Michael, additional, Kriege, Oliver, additional, Verbeek, Mareike, additional, Unglaub, Julia M., additional, Thol, Felicitas, additional, Krause, Stefan W., additional, Haenel, Mathias, additional, Neuerburg, Charlotte, additional, Vucinic, Vladan, additional, Jehn, Christian, additional, Severmann, Julia, additional, Wass, Maxi, additional, Fransecky, Lars, additional, Chemnitz, Jens, additional, Holtick, Udo, additional, Schäfer-Eckart, Kerstin, additional, Schröder, Josephine, additional, Kraus, Sabrina, additional, Krüger, William Hermann, additional, Kaiser, Ulrich, additional, Scholl, Sebastian, additional, Henning, Lea, additional, Kobbe, Guido, additional, Haas, Rainer, additional, Alakel, Nael, additional, Röhnert, Maximilian Alexander, additional, Sockel, Katja, additional, Hanoun, Maher, additional, Platzbecker, Uwe, additional, Holderried, Tobias A. W., additional, Morgner, Anke, additional, Heuser, Michael, additional, Sauer, Tim, additional, Goetze, Katharina S., additional, Wagner, Eva Maria, additional, Döhner, Konstanze, additional, Döhner, Hartmut, additional, Schliemann, Christoph, additional, Schetelig, Johannes, additional, Bornhäuser, Martin, additional, Germing, Ulrich, additional, Schroeder, Thomas, additional, and Middeke, Moritz Moritz, additional

Published
2021
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2. Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation with Venetoclax, Hypomethylating Agents and DLI - a Retrospective Multi Center Study

Author

Schuler, Esther, primary, Wagner-Drouet, Eva-Maria, additional, Ajib, Salem, additional, Bug, Gesine, additional, Crysandt, Martina, additional, Dressler, Sabine, additional, Hausmann, Andreas, additional, Heidenreich, Daniela, additional, Hirschbühl, Klaus, additional, Hoepting, Matthias, additional, Jost, Edgar, additional, Kaivers, Jennifer, additional, Klein, Stefan A, additional, Kordelas, Lambros, additional, Kriege, Oliver, additional, Mueller, Lutz Peter, additional, Rautenberg, Christina, additional, Schaffrath, Judith, additional, Schmid, Christoph, additional, Wolff, Daniel, additional, Bornhaeuser, Martin, additional, Schroeder, Thomas, additional, and Kobbe, Guido, additional

Published
2019
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3. Implementation of CMV-T-Track® in Clinical Routine to Guide Management of CMV Reactivation

Author

Wißkirchen, Jonas, Wolff, Diana, Ries, Isabelle, Kriege, Oliver, Wölfinger, Pascal, Hauptrock, Beate, Theobald, Matthias, and Wagner Drouet, Eva-Maria

Abstract

Background: Despite Letermovir prophylaxis, reactivation of cytomegalovirus (CMV), requiring close monitoring and preemptive antiviral treatment, remains to be an issue after allogeneic hematopoietic stem cell transplantation (HSCT). Monitoring CMV-specific cellular immunity can help to identify patients at risk and may guide monitoring intervals and therapeutic decisions.

Published
2023
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4. Idelalisib Impairs TREM-1 and TLR Mediated Neutrophil Activation

Author

Hasibeder, Astrid, primary, Stadler, Nicole, additional, Aranda Lopez, Pamela, additional, Desuki, Alexander, additional, Kriege, Oliver, additional, Weber, Alexander N.R., additional, Michel, Christian, additional, Teschner, Daniel, additional, Hess, Georg, additional, Theobald, Matthias, additional, and Radsak, Markus, additional

Published
2016
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5. Ibrutinib Abrogates TREM-1 Mediated Neutrophil Activation

Author

Stadler, Nicole, primary, Hasibeder, Astrid, additional, Aranda Lopez, Pamela, additional, Desuki, Alexander, additional, Kriege, Oliver, additional, Weber, Alexander N.R., additional, Michel, Christian, additional, Teschner, Daniel, additional, Hess, Georg, additional, Theobald, Matthias, additional, and Radsak, Markus, additional

Published
2016
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6. Targeting Aberrant Ncam (neural cell adhesion molecule; CD56) Expression in Acute Myeloid Leukemia

Author

Sasca, Daniel, primary, Schueler, Andrea, additional, Szybinski, Jakub, additional, Kriege, Oliver, additional, Kunz, Kerstin, additional, Fehr, Eva Marie, additional, Haehnel, Patricia, additional, Gebhardt, Wolf Henning, additional, Reid, Gerge, additional, Theobald, Matthias, additional, Bullinger, Lars, additional, and Kindler, Thomas, additional

Published
2015
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7. NCAM1 (CD56) promotes leukemogenesis and confers drug resistance in AML

Author

Sasca, Daniel, Szybinski, Jakub, Schüler, Andrea, Shah, Viral, Heidelberger, Jan, Haehnel, Patricia S., Dolnik, Anna, Kriege, Oliver, Fehr, Eva-Marie, Gebhardt, Wolf H., Reid, George, Scholl, Claudia, Theobald, Matthias, Bullinger, Lars, Beli, Petra, and Kindler, Thomas

Abstract

Neural cell adhesion molecule 1 (NCAM1; CD56) is expressed in up to 20% of acute myeloid leukemia (AML) patients. NCAM1 is widely used as a marker of minimal residual disease; however, the biological function of NCAM1 in AML remains elusive. In this study, we investigated the impact of NCAM1 expression on leukemogenesis, drug resistance, and its role as a biomarker to guide therapy. Beside t(8;21) leukemia, NCAM1 expression was found in most molecular AML subgroups at highly heterogeneous expression levels. Using complementary genetic strategies, we demonstrated an essential role of NCAM1 in the regulation of cell survival and stress resistance. Perturbation of NCAM1 induced cell death or differentiation and sensitized leukemic blasts toward genotoxic agents in vitro and in vivo. Furthermore, Ncam1 was highly expressed in leukemic progenitor cells in a murine leukemia model, and genetic depletion of Ncam1 prolonged disease latency and significantly reduced leukemia-initiating cells upon serial transplantation. To further analyze the mechanism of the NCAM1-associated phenotype, we performed phosphoproteomics and transcriptomics in different AML cell lines. NCAM1 expression strongly associated with constitutive activation of the MAPK-signaling pathway, regulation of apoptosis, or glycolysis. Pharmacological inhibition of MEK1/2 specifically inhibited proliferation and sensitized NCAM1+ AML cells to chemotherapy. In summary, our data demonstrate that aberrant expression of NCAM1 is involved in the maintenance of leukemic stem cells and confers stress resistance, likely due to activation of the MAPK pathway. Targeting MEK1/2 sensitizes AML blasts to genotoxic agents, indicating a role for NCAM1 as a biomarker to guide AML treatment.

Published
2019
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