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Your search keyword '"Dufva, Inge H"' showing total 12 results
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12 results on '"Dufva, Inge H"'

2. Epidemiologic study on survival of chronic myeloid leukemia and Ph+ acute lymphoblastic leukemia patients with BCR-ABL T315I mutation

Author

Nicolini, Franck E., Mauro, Michael J., Martinelli, Giovanni, Kim, Dong-Wook, Soverini, Simona, Müller, Martin C., Hochhaus, Andreas, Cortes, Jorge, Chuah, Charles, Dufva, Inge H., Apperley, Jane F., Yagasaki, Fumiharu, Pearson, Jay D., Peter, Senaka, Sanz Rodriguez, Cesar, Preudhomme, Claude, Giles, Francis, Goldman, John M., and Zhou, Wei

Published
2009
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4. Oral vitamin C supplementation to patients with myeloid cancer on azacitidine treatment:Normalization of plasma vitamin C induces epigenetic changes

Author

Gillberg, Linn, Ørskov, Andreas D., Nasif, Ammar, Ohtani, Hitoshi, Madaj, Zachary, Hansen, Jakob W., Rapin, Nicolas, Mogensen, Johanne B., Liu, Minmin, Dufva, Inge H., Lykkesfeldt, Jens, Hajkova, Petra, Jones, Peter A., Grønbæk, Kirsten, Gillberg, Linn, Ørskov, Andreas D., Nasif, Ammar, Ohtani, Hitoshi, Madaj, Zachary, Hansen, Jakob W., Rapin, Nicolas, Mogensen, Johanne B., Liu, Minmin, Dufva, Inge H., Lykkesfeldt, Jens, Hajkova, Petra, Jones, Peter A., and Grønbæk, Kirsten

Published
2019

5. Allogeneic stem cell transplantation for patients harboring T315I BCR-ABL mutated leukemias

Author

Nicolini, Franck Emmanuel, Basak, Grzegorz W., Soverini, Simona, Martinelli, Giovanni, Mauro, Michael J., Müller, Martin C., Hochhaus, Andreas, Chuah, Charles, Dufva, Inge H., Rege-Cambrin, Giovanna, Saglio, Giuseppe, Michallet, Mauricette, Labussière, Hélène, Morisset, Stéphane, Hayette, Sandrine, Etienne, Gabriel, Olavarria, Eduardo, Zhou, Wei, Peter, Senaka, Apperley, Jane F., and Cortes, Jorge

Published
2011
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6. The BCR-ABLT315I mutation compromises survival in chronic phase chronic myelogenous leukemia patients resistant to tyrosine kinase inhibitors, in a matched pair analysis

Author

Nicolini, Franck E, Ibrahim, Amr R, Soverini, Simona, Martinelli, Giovanni, Müller, Martin C, Hochhaus, Andreas, Dufva, Inge H, Kim, Dong-Wook, Cortes, Jorge, Mauro, Michael J, Chuah, Charles, Labussière, Hélène, Morisset, Stéphane, Roche-Lestienne, Catherine, Lippert, Eric, Hayette, Sandrine, Peter, Senaka, Zhou, Wei, Maguer-Satta, Véronique, Michallet, Mauricette, Goldman, John, Apperley, Jane F, Mahon, François-Xavier, Marin, David, Etienne, Gabriel, Nicolini, Franck E, Ibrahim, Amr R, Soverini, Simona, Martinelli, Giovanni, Müller, Martin C, Hochhaus, Andreas, Dufva, Inge H, Kim, Dong-Wook, Cortes, Jorge, Mauro, Michael J, Chuah, Charles, Labussière, Hélène, Morisset, Stéphane, Roche-Lestienne, Catherine, Lippert, Eric, Hayette, Sandrine, Peter, Senaka, Zhou, Wei, Maguer-Satta, Véronique, Michallet, Mauricette, Goldman, John, Apperley, Jane F, Mahon, François-Xavier, Marin, David, and Etienne, Gabriel

Published
2013

8. Epidemiologic study on survival of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia patients with BCR-ABL T315I mutation

Author

Nicolini, Franck E, Mauro, Michael J, Martinelli, Giovanni, Kim, Dong-Wook, Soverini, Simona, Müller, Martin C, Hochhaus, Andreas, Cortes, Jorge, Chuah, Charles, Dufva, Inge H, Apperley, Jane F, Yagasaki, Fumiharu, Pearson, Jay D, Peter, Senaka, Sanz Rodriguez, Cesar, Preudhomme, Claude, Giles, Francis, Goldman, John M, Zhou, Wei, Nicolini, Franck E, Mauro, Michael J, Martinelli, Giovanni, Kim, Dong-Wook, Soverini, Simona, Müller, Martin C, Hochhaus, Andreas, Cortes, Jorge, Chuah, Charles, Dufva, Inge H, Apperley, Jane F, Yagasaki, Fumiharu, Pearson, Jay D, Peter, Senaka, Sanz Rodriguez, Cesar, Preudhomme, Claude, Giles, Francis, Goldman, John M, and Zhou, Wei

Abstract

Udgivelsesdato: 2009-Dec, The BCR-ABL T315I mutation represents a major mechanism of resistance to tyrosine kinase inhibitors (TKIs). The objectives of this retrospective observational study were to estimate overall and progression-free survival for chronic myeloid leukemia in chronic-phase (CP), accelerated-phase (AP), or blastic-phase (BP) and Philadelphia chromosome-positive (Ph)(+) acute lymphoblastic leukemia (ALL) patients with T315I mutation. Medical records of 222 patients from 9 countries were reviewed; data were analyzed using log-rank tests and Cox proportional hazard models. Median age at T315I mutation detection was 54 years; 57% cases were men. Median time between TKI treatment initiation and T315I mutation detection was 29.2, 15.4, 5.8, and 9.1 months, respectively, for CP, AP, BP, and Ph(+) ALL patients. After T315I mutation detection, second-generation TKIs were used in 56% of cases, hydroxyurea in 39%, imatinib in 35%, cytarabine in 26%, MK-0457 in 11%, stem cell transplantation in 17%, and interferon-alpha in 6% of cases. Median overall survival from T315I mutation detection was 22.4, 28.4, 4.0, and 4.9 months, and median progression-free survival was 11.5, 22.2, 1.8, and 2.5 months, respectively, for CP, AP, BP, and Ph(+) ALL patients. These results confirm that survival of patients harboring a T315I mutation is dependent on disease phase at the time of mutation detection.

Published
2009

9. High Early Death Rate with Excellent Survival Beyond Day 30 in Acute Promyelocytic Leukemia Confirmed in Unselected Patients: Results of a Population-Based Registry Study

Author

Norgaard, Jan M., primary, Ostgard, Lene Sofie Granfeldt, additional, Kjeldsen, Eigil, additional, Holm, Mette S., additional, Kjeldsen, Lars, additional, Kallenbach, Maria, additional, Severinsen, Marianne T., additional, Johansen, Preben, additional, Friis, Lone S., additional, Weber, Duruta, additional, Kerndrup, Gitte, additional, Preiss, Birgitte, additional, Jensen, Morten K., additional, Dufva, Inge H., additional, Timshel, Susanne, additional, Andersen, Mette K., additional, and Nielsen, Ove J., additional

Published
2012
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10. The Prognostic Impact of Blast Cell Immunophenotyping in Intermediate Risk AML Patients at Diagnosis.

Author

Hoffmann, Marianne H., primary, Leinoe, Eva B., primary, Klausen, Tobias W., primary, Danielsen, Ronnie C., primary, Kjaersgaard, Erik, primary, Schmiegelow, Kjeld, primary, Hasle, Henrik, primary, Hastrup, Nina, primary, Kristensen, Jorgen S., primary, Dufva, Inge H., primary, Hansen, Niels E., primary, Bergmann, Olav J., primary, and Johnsen, Hans E., primary

Published
2004
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11. Epidemiologic study on survival of chronic myeloid leukemia and Ph+acute lymphoblastic leukemia patients with BCR-ABL T315I mutation

Author

Nicolini, Franck E., Mauro, Michael J., Martinelli, Giovanni, Kim, Dong-Wook, Soverini, Simona, Müller, Martin C., Hochhaus, Andreas, Cortes, Jorge, Chuah, Charles, Dufva, Inge H., Apperley, Jane F., Yagasaki, Fumiharu, Pearson, Jay D., Peter, Senaka, Sanz Rodriguez, Cesar, Preudhomme, Claude, Giles, Francis, Goldman, John M., and Zhou, Wei

Abstract

The BCR–ABL T315I mutation represents a major mechanism of resistance to tyrosine kinase inhibitors (TKIs). The objectives of this retrospective observational study were to estimate overall and progression-free survival for chronic myeloid leukemia in chronic-phase (CP), accelerated-phase (AP), or blastic-phase (BP) and Philadelphia chromosome—positive (Ph)+acute lymphoblastic leukemia (ALL) patients with T315I mutation. Medical records of 222 patients from 9 countries were reviewed; data were analyzed using log-rank tests and Cox proportional hazard models. Median age at T315I mutation detection was 54 years; 57% cases were men. Median time between TKI treatment initiation and T315I mutation detection was 29.2, 15.4, 5.8, and 9.1 months, respectively, for CP, AP, BP, and Ph+ALL patients. After T315I mutation detection, second-generation TKIs were used in 56% of cases, hydroxyurea in 39%, imatinib in 35%, cytarabine in 26%, MK-0457 in 11%, stem cell transplantation in 17%, and interferon-α in 6% of cases. Median overall survival from T315I mutation detection was 22.4, 28.4, 4.0, and 4.9 months, and median progression-free survival was 11.5, 22.2, 1.8, and 2.5 months, respectively, for CP, AP, BP, and Ph+ALL patients. These results confirm that survival of patients harboring a T315I mutation is dependent on disease phase at the time of mutation detection.

Published
2009
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12. The BCR-ABLT315I mutation compromises survival in chronic phase chronic myelogenous leukemia patients resistant to tyrosine kinase inhibitors, in a matched pair analysis.

Author

Nicolini FE, Ibrahim AR, Soverini S, Martinelli G, Müller MC, Hochhaus A, Dufva IH, Kim DW, Cortes J, Mauro MJ, Chuah C, Labussière H, Morisset S, Roche-Lestienne C, Lippert E, Hayette S, Peter S, Zhou W, Maguer-Satta V, Michallet M, Goldman J, Apperley JF, Mahon FX, Marin D, and Etienne G

Subjects
Adolescent, Adult, Aged, Cohort Studies, Drug Resistance, Neoplasm genetics, Female, Humans, Leukemia, Myeloid, Chronic-Phase mortality, Male, Middle Aged, Prospective Studies, Protein Kinase Inhibitors pharmacology, Retrospective Studies, Survival Rate, Young Adult, Fusion Proteins, bcr-abl genetics, Genes, abl, Leukemia, Myeloid, Chronic-Phase drug therapy, Leukemia, Myeloid, Chronic-Phase genetics, Mutation, Protein Kinase Inhibitors therapeutic use
Abstract

The BCR-ABL T315I mutation confers resistance to currently licensed tyrosine kinase inhibitors in chronic myelogenous leukemia. However, the impact of this mutation on survival in early stages of disease, in chronic phase, has never been detailed. Using matched pair analysis, a cohort of 64 patients with chronic phase chronic myelogenous leukemia harboring a T315I mutation and resistant to imatinib mesylate was compared to a similar cohort of 53 chronic phase patients resistant to imatinib, but with no detectable T315I mutation, in the pre-ponatinib era. These patients were matched according to age at diagnosis, interval between disease diagnosis and start of imatinib treatment, and duration of imatinib therapy. Kaplan-Meier survival analyses demonstrated the significant negative impact of the presence of the T315I mutation on overall survival (since imatinib-resistance: 48.4 months for T315I(+) patients versus not reached for T315I(-) ones; P=0.006) and failure-free survival (since imatinib-resistance: 34.7 months for T315I(+) patients versus not reached for T315I(-) patients; P=0.003). In addition, Cox proportional hazard models adjusted on overall survival demonstrated the negative influence of the T315I mutation (P=0.02, HR=2.54). These results confirm early assumptions concerning the poor prognosis of chronic phase chronic myelogenous leukemia patients with the T315I mutation who are not eligible for allogeneic transplantation, and demonstrate the need for more therapeutic options.

Published
2013
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