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7 results on '"Becker, Natalia"'

2. Salvage Autologous Transplant and Lenalidomide Maintenance Versus Continuous Lenalidomide/Dexamethasone for Relapsed Multiple Myeloma: Results of the Randomized GMMG Phase III Multicenter Trial Relapse

Author

Goldschmidt, Hartmut, primary, Baertsch, Marc-A., additional, Schlenzka, Jana, additional, Becker, Natalia, additional, Christina, Habermehl, additional, Hielscher, Thomas, additional, Raab, Marc S, additional, Hillengass, Jens, additional, Müller-Tidow, Carsten, additional, Luntz, Steffen, additional, Jauch, Anna, additional, Brossart, Peter, additional, Goerner, Martin, additional, Klein, Stefan A, additional, Schmidt-Hieber, Martin, additional, Reimer, Peter, additional, Graeven, Ullrich, additional, Fenk, Roland, additional, Haenel, Mathias, additional, Martin, Hans, additional, Lindemann, Hans-Walter, additional, Scheid, Christoph, additional, Nogai, Axel, additional, Salwender, Hans Jürgen, additional, Noppeney, Richard, additional, and Weisel, Katja, additional

Published
2018
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4. Evaluation of Stem Cell Mobilization in Patients with Multiple Myeloma after Lenalidomide-Based Induction Chemotherapy within the GMMG-HD6 Trial

Author

Wuchter, Patrick, primary, Bertsch, Uta, additional, Salwender, Hans-Juergen, additional, Munder, Markus, additional, Haenel, Mathias, additional, Benner, Axel, additional, Becker, Natalia, additional, Fenk, Roland, additional, Duerig, Jan, additional, Blau, Igor Wolfgang, additional, Lisenko, Katharina, additional, Hillengass, Jens, additional, Raab, Marc S., additional, Baertsch, Marc Andrea, additional, Seidel-Glaetzer, Andrea, additional, Ho, Anthony D, additional, Graeven, Ullrich, additional, Scheid, Christof, additional, Weisel, Katja, additional, and Goldschmidt, Hartmut, additional

Published
2016
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5. Pre-Transplant Weight Loss Influences Outcome of Patients with Myelodysplastic Syndrome Undergoing Allogeneic Stem Cell Transplantation

Author

Radujkovic, Aleksandar, primary, Becker, Natalia, additional, Benner, Axel, additional, Dietrich, Sascha, additional, Penack, Olaf, additional, Platzbecker, Uwe, additional, Stölzel, Friedrich, additional, Bornhäuser, Martin, additional, Hegenbart, Ute, additional, Ho, Anthony D, additional, Dreger, Peter, additional, and Luft, Thomas, additional

Published
2014
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6. High-resolution genomic profiling of childhood T-ALL reveals frequent copy-number alterations affecting the TGF-β and PI3K-AKT pathways and deletions at 6q15-16.1 as a genomic marker for unfavorable early treatment response

Author

Remke, Marc, primary, Pfister, Stefan, additional, Kox, Corinne, additional, Toedt, Grischa, additional, Becker, Natalia, additional, Benner, Axel, additional, Werft, Wiebke, additional, Breit, Stephen, additional, Liu, Shuangyou, additional, Engel, Felix, additional, Wittmann, Andrea, additional, Zimmermann, Martin, additional, Stanulla, Martin, additional, Schrappe, Martin, additional, Ludwig, Wolf-Dieter, additional, Bartram, Claus R., additional, Radlwimmer, Bernhard, additional, Muckenthaler, Martina U., additional, Lichter, Peter, additional, and Kulozik, Andreas E., additional

Published
2009
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7. High-resolution genomic profiling of childhood T-ALL reveals frequent copy-number alterations affecting the TGF-beta and PI3K-AKT pathways and deletions at 6q15-16.1 as a genomic marker for unfavorable early treatment response.

Author

Remke M, Pfister S, Kox C, Toedt G, Becker N, Benner A, Werft W, Breit S, Liu S, Engel F, Wittmann A, Zimmermann M, Stanulla M, Schrappe M, Ludwig WD, Bartram CR, Radlwimmer B, Muckenthaler MU, Lichter P, and Kulozik AE

Subjects
Adolescent, Child, Child, Preschool, Chromosomes, Human, Pair 6 ultrastructure, Comparative Genomic Hybridization, Cyclin-Dependent Kinase Inhibitor p27, Female, Gene Dosage, Humans, Intracellular Signaling Peptides and Proteins genetics, Male, Multicenter Studies as Topic statistics & numerical data, Phosphatidylinositol 3-Kinases genetics, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma drug therapy, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma mortality, Prognosis, Proto-Oncogene Proteins c-akt genetics, Receptor, Notch1 genetics, Transforming Growth Factor beta genetics, Treatment Outcome, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Chromosome Deletion, Chromosomes, Human, Pair 6 genetics, Neoplasm Proteins genetics, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma genetics, Signal Transduction genetics
Abstract

Precursor T-cell acute lymphoblastic leukemia (T-ALL) in children represents a clinical challenge, because relapses are usually fatal. It is thus necessary to identify high-risk patients as early as possible to effectively individualize treatment. We aimed to define novel molecular risk markers in T-ALL and performed array-based comparative genomic hybridization (array-CGH) and expression analyses in 73 patients. We show that DNA copy-number changes are common in T-ALL and affect 70 of 73 (96%) patients. Notably, genomic imbalances predicted to down-regulate the TGF-beta or up-regulate the PI3K-AKT pathways are identified in 25 of 73 (34%) and 21 of 73 (29%) patients, suggesting that these pathways play key roles in T-ALL leukemogenesis. Furthermore, we identified a deletion at 6q15-16.1 in 9 of 73 (12%) of the patients, which predicts poor early treatment response. This deletion includes the CASP8AP2 gene, whose expression is shown to be down-regulated. The interaction of CASP8AP2 with CASP8 plays a crucial role in apoptotic regulation, suggesting a functional link between the clinical effect of the deletion and the molecular mode of action. The data presented here implicate the TGF-beta and PI3K-AKT pathways in T-ALL leukemogenesis and identify a subgroup of patients with CASP8AP2 deletions and poor early treatment response.

Published
2009
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