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29 results on '"Habdank, Marianne"'

1. TP53 alterations in acute myeloid leukemia with complex karyotype correlate with specific copy number alterations, monosomal karyotype, and dismal outcome

Author

Rücker, Frank G., Schlenk, Richard F., Bullinger, Lars, Kayser, Sabine, Teleanu, Veronica, Kett, Helena, Habdank, Marianne, Kugler, Carla-Maria, Holzmann, Karlheinz, Gaidzik, Verena I., Paschka, Peter, Held, Gerhard, von Lilienfeld-Toal, Marie, Lübbert, Michael, Fröhling, Stefan, Zenz, Thorsten, Krauter, Jürgen, Schlegelberger, Brigitte, Ganser, Arnold, Lichter, Peter, Döhner, Konstanze, and Döhner, Hartmut

Published
2012
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2. Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia

Author

Schlenk, Richard F., Dohner, Konstanze, Krauter, Jurgen, Frohling, Stefan, Corbacioglu, Andrea, Bullinger, Lars, Habdank, Marianne, Spath, Daniela, Morgan, Michael, Benner, Axel, Schlegelberger, Brigette, Heil, Gerhard, Ganser, Arnold, and Dohner, Hartmut

Subjects
Gene mutations -- Health aspects, Myelocytic leukemia -- Genetic aspects, Myelocytic leukemia -- Care and treatment, Nonlymphoid leukemia -- Genetic aspects, Nonlymphoid leukemia -- Care and treatment
Abstract

A study to determine the mutations that occur in several genes that could be a cause of acute myeloid leukemia and the effects on treatment is conducted. Results showed that the mutation of the genes did have an effect on the outcome of treatment for patients suffering from leukemia.

Published
2008

3. CDK4/6 Inhibitor Palbociclib for Treatment of KMT2A-Rearranged Acute Myeloid Leukemia: Interim Analysis of the AMLSG 23-14 Trial

Author

Fröhling, Stefan, primary, Agrawal, Mridul, additional, Jahn, Nikolaus, additional, Fransecky, Lars R., additional, Baldus, Claudia D., additional, Wäsch, Ralph, additional, Lübbert, Michael, additional, Walter, Gina, additional, Jensen, Patrizia, additional, Scholl, Claudia, additional, Habdank, Marianne, additional, Döhner, Konstanze, additional, Döhner, Hartmut, additional, and Schlenk, Richard F., additional

Published
2016
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4. Clinical Relevance of Alternatively Spliced Isoform AML1-ETO9a in Adult Patients with t(8;21)(q22;q22.1) Acute Myeloid Leukemia (AML): A Study of the German-Austrian AML Study Group (AMLSG)

Author

Agrawal, Mridul, Corbacioglu, Andrea, Weber, Daniela, Gaidzik, Verena I., Habdank, Marianne, Jahn, Nikolaus, Schroeder, Thomas Michael, Kindler, Thomas, Wattad, Mohammed Amen, Lübbert, Michael, Fiedler, Walter, Götze, Katharina S., Ringhoffer, Mark, Schleicher, Jan, Lange, Elisabeth, Pfreundschuh, Michael, Griesshammer, Martin, Greil, Richard, Kirchen, Heinz, Koller, Elisabeth, Thol, Felicitas, Krauter, Jurgen, Schlenk, Richard F., Heuser, Michael, Ganser, Arnold, Bullinger, Lars, Paschka, Peter, Döhner, Hartmut, and Döhner, Konstanze

Published
2017
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5. TET2 Mutations in Acute Myeloid Leukemia (AML): Results From a Comprehensive Genetic and Clinical Analysis of the AML Study Group

Author

Gaidzik, Verena I., primary, Paschka, Peter, additional, Späth, Daniela, additional, Habdank, Marianne, additional, Köhne, Claus-Henning, additional, Germing, Ulrich, additional, von Lilienfeld-Toal, Marie, additional, Held, Gerhard, additional, Horst, Heinz-August, additional, Haase, Detlef, additional, Bentz, Martin, additional, Götze, Katharina, additional, Döhner, Hartmut, additional, Schlenk, Richard F., additional, Bullinger, Lars, additional, and Döhner, Konstanze, additional

Published
2012
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6. ASXL1 Mutations Predict for Resistance to Chemotherapy and Inferior Outcome in Younger Adult Patients with Acute Myeloid Leukemia (AML): A Study of the German-Austrian AMLSG

Author

Paschka, Peter, primary, Schlenk, Richard F., additional, Herzig, Julia, additional, Aulitzky, Teresa, additional, Gaidzik, Verena I., additional, Bullinger, Lars, additional, Habdank, Marianne, additional, Corbacioglu, Andrea, additional, Späth, Daniela, additional, Köhne, Claus-Henning, additional, Kündgen, Andrea, additional, von Lilienfeld-Toal, Marie, additional, Held, Gerhard, additional, Horst, Heinz A., additional, Götze, Katharina, additional, Bentz, Martin, additional, Krauter, Jürgen, additional, Ganser, Arnold, additional, Döhner, Hartmut, additional, and Döhner, Konstanze, additional

Published
2011
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7. TP53 Alterations in Acute Myeloid Leukemia with Complex Karyotype Correlate with Specific Copy Number Alterations, Monosomal Karyotype, and Dismal Outcome,

Author

Rücker, Frank G., primary, Schlenk, Richard F., additional, Bullinger, Lars, additional, Kayser, Sabine, additional, Teleanu, Veronica, additional, Kett, Helena, additional, Habdank, Marianne, additional, Kugler, Carla-Maria, additional, Holzmann, Karlheinz, additional, Gaidzik, Verena I., additional, Paschka, Peter, additional, Held, Gerhard, additional, von Lilienfeld-Toal, Marie, additional, Lübbert, Michael, additional, Fröhling, Stefan, additional, Zenz, Thorsten, additional, Krauter, Jürgen, additional, Schlegelberger, Brigitte, additional, Ganser, Arnold, additional, Lichter, Peter, additional, Döhner, Konstanze, additional, and Döhner, Hartmut, additional

Published
2011
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8. Monitoring of Minimal Residual Disease in NPM1-Mutated Acute Myeloid Leukemia: A Study From the German-Austrian Acute Myeloid Leukemia Study Group

Author

Krönke, Jan, primary, Schlenk, Richard F., additional, Jensen, Kai-Ole, additional, Tschürtz, Florian, additional, Corbacioglu, Andrea, additional, Gaidzik, Verena I., additional, Paschka, Peter, additional, Onken, Shiva, additional, Eiwen, Karina, additional, Habdank, Marianne, additional, Späth, Daniela, additional, Lübbert, Michael, additional, Wattad, Mohammed, additional, Kindler, Thomas, additional, Salih, Helmut R., additional, Held, Gerhard, additional, Nachbaur, David, additional, von Lilienfeld-Toal, Marie, additional, Germing, Ulrich, additional, Haase, Detlef, additional, Mergenthaler, Hans-Günther, additional, Krauter, Jürgen, additional, Ganser, Arnold, additional, Göhring, Gudrun, additional, Schlegelberger, Brigitte, additional, Döhner, Hartmut, additional, and Döhner, Konstanze, additional

Published
2011
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9. TET2 Mutations In Acute Myeloid Leukemia (AML): Results on 783 Patients Treated within the AML HD98A Study of the AML Study Group (AMLSG)

Author

Gaidzik, Verena I., primary, Schlenk, Richard F., additional, Paschka, Peter, additional, Köhne, Claus-Henning, additional, Held, Gerhard, additional, Habdank, Marianne, additional, Gohlke, Juliane, additional, Mergenthaler, Hans-Günther, additional, Salwender, Hans J., additional, Bullinger, Lars, additional, Döhner, Hartmut, additional, and Döhner, Konstanze, additional

Published
2010
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10. IDH1 and IDH2 Mutations Are Frequent Genetic Alterations in Acute Myeloid Leukemia and Confer Adverse Prognosis in Cytogenetically Normal Acute Myeloid Leukemia With NPM1 Mutation Without FLT3 Internal Tandem Duplication

Author

Paschka, Peter, primary, Schlenk, Richard F., additional, Gaidzik, Verena I., additional, Habdank, Marianne, additional, Krönke, Jan, additional, Bullinger, Lars, additional, Späth, Daniela, additional, Kayser, Sabine, additional, Zucknick, Manuela, additional, Götze, Katharina, additional, Horst, Heinz-A., additional, Germing, Ulrich, additional, Döhner, Hartmut, additional, and Döhner, Konstanze, additional

Published
2010
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11. Identification of Clinically Relevant Predictive MRD Checkpoints in AML Patients with NPM1 Mutations: A Study of the AML Study Group (AMLSG).

Author

Krönke, Jan, primary, Schlenk, Richard, additional, Jensen, Kai-Ole, additional, Eiwen, Karina, additional, Habdank, Marianne, additional, Späth, Daniela, additional, Krauter, Jürgen, additional, Ganser, Arnold, additional, Göhring, Gudrun, additional, Schlegelberger, Brigitte, additional, Döhner, Hartmut, additional, and Döhner, Konstanze, additional

Published
2009
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13. The Genotype NPM1mut/FLT3-ITDneg Is a Highly Significant Predictive Factor for Response to Therapy with All-Trans Retinoic Acid in Acute Myeloid Leukemia - Results from AMLSG Trial AML HD98B.

Author

Schlenk, Richard F., primary, Döhner, Konstanze, additional, Kneba, Michael, additional, Valle, Francesco del, additional, Hartmann, Frank, additional, Kirchen, Heinz, additional, Koller, Elisabeth, additional, Götze, Katharina, additional, Fischer, Jörg Th., additional, Habdank, Marianne, additional, Späth, Daniela, additional, Groner, Silja, additional, Corbacioglu, Andrea, additional, Benner, Axel, additional, Fröhling, Stefan, additional, and Döhner, Hartmut, additional

Published
2007
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14. Clinical Impact of WT1 Mutations in the Context of Other Molecular Markers in Cytogenetically Normal Acute Myeloid Leukemia (AML): A Study of the German-Austrian AML Study Group (AMLSG).

Author

Gaidzik, Verena I., primary, Habdank, Marianne, primary, Moschny, Simone, primary, Groner, Silja, primary, Spath, Daniela, primary, Krauter, Jurgen, primary, Schlegelberger, Brigitte, primary, Ganser, Arnold, primary, Dohner, Hartmut, primary, Schlenk, Richard F., primary, and Dohner, Konstanze, primary

Published
2007
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19. TP53alterations in acute myeloid leukemia with complex karyotype correlate with specific copy number alterations, monosomal karyotype, and dismal outcome

Author

Rücker, Frank G., Schlenk, Richard F., Bullinger, Lars, Kayser, Sabine, Teleanu, Veronica, Kett, Helena, Habdank, Marianne, Kugler, Carla-Maria, Holzmann, Karlheinz, Gaidzik, Verena I., Paschka, Peter, Held, Gerhard, von Lilienfeld-Toal, Marie, Lübbert, Michael, Fröhling, Stefan, Zenz, Thorsten, Krauter, Jürgen, Schlegelberger, Brigitte, Ganser, Arnold, Lichter, Peter, Döhner, Konstanze, and Döhner, Hartmut

Abstract

To assess the frequency of TP53alterations and their correlation with other genetic changes and outcome in acute myeloid leukemia with complex karyotype (CK-AML), we performed integrative analysis using TP53mutational screening and array-based genomic profiling in 234 CK-AMLs. TP53mutations were found in 141 of 234 (60%) and TP53losses were identified in 94 of 234 (40%) CK-AMLs; in total, 164 of 234 (70%) cases had TP53alterations. TP53-altered CK-AML were characterized by a higher degree of genomic complexity (aberrations per case, 14.30 vs 6.16; P< .0001) and by a higher frequency of specific copy number alterations, such as −5/5q−, −7/7q−, −16/16q−, −18/18q−, +1/+1p, and +11/+11q/amp11q13∼25; among CK-AMLs, TP53-altered more frequently exhibited a monosomal karyotype (MK). Patients with TP53alterations were older and had significantly lower complete remission rates, inferior event-free, relapse-free, and overall survival. In multivariable analysis for overall survival, TP53alterations, white blood cell counts, and age were the only significant factors. In conclusion, TP53is the most frequently known altered gene in CK-AML. TP53alterations are associated with older age, genomic complexity, specific DNA copy number alterations, MK, and dismal outcome. In multivariable analysis, TP53alteration is the most important prognostic factor in CK-AML, outweighing all other variables, including the MK category.

Published
2012
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20. Mutant nucleophosmin (NPM1)predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations

Author

Döhner, Konstanze, Schlenk, Richard F., Habdank, Marianne, Scholl, Claudia, Rücker, Frank G., Corbacioglu, Andrea, Bullinger, Lars, Fröhling, Stefan, and Döhner, Hartmut

Abstract

To assess the prognostic relevance of mutations in the NPM1gene encoding a nucleocytoplasmic shuttle protein in younger adults with acute myeloid leukemia (AML) and normal cytogenetics, sequencing of NPM1exon 12 was performed in diagnostic samples from 300 patients entered into 2 consecutive multicenter trials of the AML Study Group (AMLSG). Treatment included intensive double-induction therapy and consolidation therapy with high cumulative doses of high-dose cytarabine. NPM1mutations were identified in 48% of the patients including 12 novel sequence variants, all leading to a frameshift in the C-terminus of the nucleophosmin 1 (NPM1) protein. Mutant NPM1was associated with specific clinical, phenotypical, and genetic features. Statistical analysis revealed a significant interaction of NPM1and FLT3internal tandem duplications (ITDs). NPM1mutations predicted for better response to induction therapy and for favorable overall survival (OS) only in the absence of FLT3ITD. Multivariable analysis for OS revealed combined NPM1-mutated/FLT3ITD–negative status, CEBPAmutation status, availability of a human leukocyte antigen (HLA)–compatible donor, secondary AML, and lactate dehydrogenase (LDH) as prognostic factors. In conclusion, NPM1mutations in the absence of FLT3ITD define a distinct molecular and prognostic subclass of young-adult AML patients with normal cytogenetics.

Published
2005
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21. Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations

Author

Döhner, Konstanze, Schlenk, Richard F., Habdank, Marianne, Scholl, Claudia, Rücker, Frank G., Corbacioglu, Andrea, Bullinger, Lars, Fröhling, Stefan, and Döhner, Hartmut

Abstract

To assess the prognostic relevance of mutations in the NPM1 gene encoding a nucleocytoplasmic shuttle protein in younger adults with acute myeloid leukemia (AML) and normal cytogenetics, sequencing of NPM1 exon 12 was performed in diagnostic samples from 300 patients entered into 2 consecutive multicenter trials of the AML Study Group (AMLSG). Treatment included intensive double-induction therapy and consolidation therapy with high cumulative doses of high-dose cytarabine. NPM1 mutations were identified in 48% of the patients including 12 novel sequence variants, all leading to a frameshift in the C-terminus of the nucleophosmin 1 (NPM1) protein. Mutant NPM1 was associated with specific clinical, phenotypical, and genetic features. Statistical analysis revealed a significant interaction of NPM1 and FLT3 internal tandem duplications (ITDs). NPM1 mutations predicted for better response to induction therapy and for favorable overall survival (OS) only in the absence of FLT3 ITD. Multivariable analysis for OS revealed combined NPM1-mutated/FLT3 ITD–negative status, CEBPA mutation status, availability of a human leukocyte antigen (HLA)–compatible donor, secondary AML, and lactate dehydrogenase (LDH) as prognostic factors. In conclusion, NPM1 mutations in the absence of FLT3 ITD define a distinct molecular and prognostic subclass of young-adult AML patients with normal cytogenetics.

Published
2005
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22. Clinical Relevance of Alternatively Spliced Isoform AML1-ETO9ain Adult Patients with t(8;21)(q22;q22.1) Acute Myeloid Leukemia (AML): A Study of the German-Austrian AML Study Group (AMLSG)

Author

Agrawal, Mridul, Corbacioglu, Andrea, Weber, Daniela, Gaidzik, Verena I., Habdank, Marianne, Jahn, Nikolaus, Schroeder, Thomas Michael, Kindler, Thomas, Wattad, Mohammed Amen, Lübbert, Michael, Fiedler, Walter, Götze, Katharina S., Ringhoffer, Mark, Schleicher, Jan, Lange, Elisabeth, Pfreundschuh, Michael, Griesshammer, Martin, Greil, Richard, Kirchen, Heinz, Koller, Elisabeth, Thol, Felicitas, Krauter, Jurgen, Schlenk, Richard F., Heuser, Michael, Ganser, Arnold, Bullinger, Lars, Paschka, Peter, Döhner, Hartmut, and Döhner, Konstanze

Abstract

Background:AML with t(8;21)(q22;q22.1) defines a distinct disease entity within the WHO category ‘AML with recurrent genetic abnormalities’ and results in the formation of the AML1-ETO(AE) fusion transcript. Recent data showed that alternative splicing generates a truncated variant of AE, namely AML1-ETO9a(AE9a), containing an additional exon 9a. Co-expression of AEand AE9awas shown to induce a more aggressive leukemic phenotype with a rapid onset of AML in a retrovirally transduced mouse model (Yan et al., Nat Med2006). However, the clinical relevance of the alternatively spliced AE9aisoform in adult patients (pts) with t(8;21) AML is not well determined yet.

Published
2017
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23. ASXL1Mutations Predict for Resistance to Chemotherapy and Inferior Outcome in Younger Adult Patients with Acute Myeloid Leukemia (AML): A Study of the German-Austrian AMLSG

Author

Paschka, Peter, Schlenk, Richard F., Herzig, Julia, Aulitzky, Teresa, Gaidzik, Verena I., Bullinger, Lars, Habdank, Marianne, Corbacioglu, Andrea, Späth, Daniela, Köhne, Claus-Henning, Kündgen, Andrea, von Lilienfeld-Toal, Marie, Held, Gerhard, Horst, Heinz A., Götze, Katharina, Bentz, Martin, Krauter, Jürgen, Ganser, Arnold, Döhner, Hartmut, and Döhner, Konstanze

Abstract

Abstract 412

Published
2011
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24. TP53Alterations in Acute Myeloid Leukemia with Complex Karyotype Correlate with Specific Copy Number Alterations, Monosomal Karyotype, and Dismal Outcome,

Author

Rücker, Frank G., Schlenk, Richard F., Bullinger, Lars, Kayser, Sabine, Teleanu, Veronica, Kett, Helena, Habdank, Marianne, Kugler, Carla-Maria, Holzmann, Karlheinz, Gaidzik, Verena I., Paschka, Peter, Held, Gerhard, von Lilienfeld-Toal, Marie, Lübbert, Michael, Fröhling, Stefan, Zenz, Thorsten, Krauter, Jürgen, Schlegelberger, Brigitte, Ganser, Arnold, Lichter, Peter, Döhner, Konstanze, and Döhner, Hartmut

Abstract

Abstract 3558

Published
2011
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27. Monitoring of Minimal Residual Disease in NPM1Mutated Acute Myeloid Leukemia (AML): Results of the AML Study Group (AMLSG)

Author

Krönke, Jan, Schlenk, Richard, Jensen, Kai-Ole, Eiwen, Karina, Habdank, Marianne, Späth, Daniela, Krauter, Jürgen, Ganser, Arnold, Döhner, Hartmut, and Döhner, Konstanze

Abstract

Background:Mutations in the nucleophosmin 1 (NPM1) gene represent the most frequent gene mutations in acute myeloid leukemia (AML), with highest frequency (50–60%) in cytogenetic normal (CN)-AML and these mutations can be used as molecular markers for monitoring of minimal residual disease (MRD).

Published
2008
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28. High-resolution single-nucleotide polymorphism array-profiling in myeloproliferative neoplasms identifies novel genomic aberrations.

Author

Stegelmann F, Bullinger L, Griesshammer M, Holzmann K, Habdank M, Kuhn S, Maile C, Schauer S, Döhner H, and Döhner K

Subjects
Chromosomes, Human genetics, Genome, Human, Humans, Janus Kinase 2 genetics, Middle Aged, Mutation genetics, Neurofibromatosis 1 genetics, Oligonucleotide Array Sequence Analysis, Chromosome Aberrations, Gene Expression Profiling, Myeloproliferative Disorders genetics, Polymorphism, Single Nucleotide genetics
Abstract

Single-nucleotide polymorphism arrays allow for genome-wide profiling of copy-number alterations and copy-neutral runs of homozygosity at high resolution. To identify novel genetic lesions in myeloproliferative neoplasms, a large series of 151 clinically well characterized patients was analyzed in our study. Copy-number alterations were rare in essential thrombocythemia and polycythemia vera. In contrast, approximately one third of myelofibrosis patients exhibited small genomic losses (less than 5 Mb). In 2 secondary myelofibrosis cases the tumor suppressor gene NF1 in 17q11.2 was affected. Sequencing analyses revealed a mutation in the remaining NF1 allele of one patient. In terms of copy-neutral aberrations, no chromosomes other than 9p were recurrently affected. In conclusion, novel genomic aberrations were identified in our study, in particular in patients with myelofibrosis. Further analyses on single-gene level are necessary to uncover the mechanisms that are involved in the pathogenesis of myeloproliferative neoplasms.

Published
2010
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29. Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with acute myeloid leukemia. Results from the AMLSG Trial AML HD98B.

Author

Schlenk RF, Döhner K, Kneba M, Götze K, Hartmann F, Del Valle F, Kirchen H, Koller E, Fischer JT, Bullinger L, Habdank M, Späth D, Groner S, Krebs B, Kayser S, Corbacioglu A, Anhalt A, Benner A, Fröhling S, and Döhner H

Subjects
Aged, Aged, 80 and over, Biomarkers metabolism, Disease-Free Survival, Female, Humans, Leukemia, Myeloid, Acute metabolism, Male, Middle Aged, Nucleophosmin, Pilot Projects, Survival Rate, Treatment Outcome, Leukemia, Myeloid, Acute drug therapy, Leukemia, Myeloid, Acute genetics, Mutation genetics, Tretinoin therapeutic use
Abstract

Background: In a previous randomized trial, AML HD98B, we showed that administration of all-trans retinoic acid in addition to intensive chemotherapy improved the outcome of older patients with acute myeloid leukemia. The objectives of this study were to evaluate the prognostic impact of gene mutations and to identify predictive genetic factors for the all-trans retinoic acid treatment effect., Design and Methods: Data from mutation analyses of the NPM1, CEBPA, FLT3, and MLL genes were correlated with outcome in patients 61 years and older treated within the AML HD98B trial., Results: The frequencies of mutations were: NPM1, 23%; CEBPA, 8.5% (analysis restricted to patients with a normal karyotype); FLT3 internal tandem duplications (ITD), 17%; FLT3 tyrosine kinase domain mutations, 5%; and MLL partial tandem duplications, 4.5%. The genotype mutant NPM1 was positively and adverse cytogenetics as well as higher white blood cell count negatively correlated with achievement of complete remission. In Cox regression analysis, a significant interaction between the genotype mutant NPM1 without FLT3-ITD and treatment with all-trans retinoic acid was identified, in that the beneficial effect of all-trans retinoic acid on relapse-free and overall survival was restricted to this subgroup of patients. Other significant factors for survival were age, adverse cytogenetics, and logarithm of white cell count., Conclusions: In elderly patients with acute myeloid leukemia, NPM1 mutations are associated with achievement of complete remission, and the genotype 'mutant NPM1 without FLT3-ITD' appears to be a predictive marker for response to all-trans retinoic acid given as an adjunct to intensive chemotherapy (ClinicalTrials.gov Identifier: NCT00151242).

Published
2009
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