14 results on '"Lafage-Pochitaloff, M."'
Search Results
2. Generation of potent T(h)1 responses from patients with lymphoid malignancies after differentiation of B lymphocytes into dendritic-like cells.
- Author
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Mohty M, Isnardon D, Charbonnier A, Lafage-Pochitaloff M, Merlin M, Sainty D, Olive D, and Gaugler B
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- Adult, Aged, Aged, 80 and over, Antigens, CD19 analysis, B-Lymphocytes drug effects, CD4-Positive T-Lymphocytes immunology, CD40 Ligand pharmacology, Cell Differentiation, Cell Division, Cells, Cultured, Child, Preschool, Female, Humans, Interleukin-4 pharmacology, L-Selectin metabolism, Leukemia therapy, Leukemia, Lymphocytic, Chronic, B-Cell immunology, Leukemia, Plasma Cell immunology, Male, Middle Aged, Precursor Cell Lymphoblastic Leukemia-Lymphoma immunology, Receptors, CCR7, Receptors, Chemokine metabolism, B-Lymphocytes immunology, Dendritic Cells immunology, Interferon-gamma biosynthesis, Leukemia immunology
- Abstract
Dendritic cells (DC) are a group of potent antigen-presenting cells (APC) specialized for initiating T cell immune responses. They originate from the bone marrow and upon stimulation with bacterial products, cytokines or CD40 ligation they acquire the ability to migrate to the secondary lymphoid organs. In vitro DC can be generated from human CD34(+) bone marrow cells and CD14(+) peripheral blood monocytes after culture with different cytokine combinations. Since most leukemic cells and tumors in general are devoid of APC capacities, various strategies have been used to increase their recognition and confer the capacity of antigen presentation on them. Because of our interest in the design of vaccine immunotherapy protocols for the adjuvant treatment of patients with lymphoid malignancies (LM), we chose to explore the capacity of human acute lymphoblastic leukemia, chronic lymphocytic leukemia and plasma cell leukemia to differentiate into cells with APC and DC features. Our results among a sample of 10 patients demonstrate that such approach is feasible. Leukemic cells could be induced in the presence of IL-4 and CD40L to exhibit a DC morphology with a phenotype of mature DC-like cells. They could also induce a potent proliferative response in naive CD4(+) T cells. In addition, they expressed chemokine receptor CCR7 and CD62L, and could drive T cells towards a T(h)1 response with secretion of IFN-gamma. Our strategy leading to increased LM cell immunogenicity may have potential clinical applications and LM appear to be attracting candidates for adjuvant vaccination and adoptive immunotherapy.
- Published
- 2002
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3. CD4(+), CD56(+) DC2 acute leukemia is characterized by recurrent clonal chromosomal changes affecting 6 major targets: a study of 21 cases by the Groupe Français de Cytogénétique Hématologique.
- Author
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Leroux D, Mugneret F, Callanan M, Radford-Weiss I, Dastugue N, Feuillard J, Le Mée F, Plessis G, Talmant P, Gachard N, Uettwiller F, Pages MP, Mozziconacci MJ, Eclache V, Sibille C, Avet-Loiseau H, and Lafage-Pochitaloff M
- Subjects
- Acute Disease, Adolescent, Aged, Aged, 80 and over, Child, Female, Humans, In Situ Hybridization, Fluorescence, Karyotyping, Leukemia immunology, Male, Middle Aged, CD4 Antigens analysis, CD56 Antigen analysis, Chromosome Aberrations, Leukemia genetics
- Abstract
CD4(+), CD56(+) DC2 malignancies constitute a novel disease entity, which has recently been shown to arise from a transformed lymphoid-related plasmacytoid dendritic cell (DC2). Diagnosis is primarily based on a particular immunophenotype with tumor cells expressing CD4 and CD56 antigens in the absence of common lymphoid or myeloid lineage markers. Little is currently known about the cytogenetic features of this disease entity. In this setting, the Groupe Français de Cytogénétique Hématologique (GFCH) initiated a cytogenetic study of 18 adults and 3 children with CD4(+), CD56(+) DC2 acute leukemia using conventional and fluorescence in situ hybridization/24-color karyotyping. Clonal, mostly complex chromosome aberrations were found in 14 patients (66%). Six major recurrent chromosomal targets were defined. These were 5q, 12p, 13q, 6q, 15q, and 9, which were involved in 72% (5q), 64% (12p and 13q), 50% (6q), 43% (15q), and 28% (monosomy 9) of cases, respectively. Cytogenetic features can be summarized as follows: (1) gross genomic imbalances (mostly losses) predominate, (2) no single anomaly can be considered as specific, whereas their combination/accumulation is, and (3) both lymphoid and myeloid lineage-associated rearrangements are observed in unusual combinations in the same cell. This is suggestive of complex multistep tumorigenic mechanisms and is supportive of the hypothesis that CD4(+), CD56(+) DC2 acute leukemia may arise from an undifferentiated nonmyeloid nonlymphoid progenitor cell. In conclusion, the present study documents for the first time the existence of a characteristic cytogenetic profile for this novel disease entity.
- Published
- 2002
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4. NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique
- Author
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Romana, S P, Radford-Weiss, I, Ben Abdelali, R, Schluth, C, Petit, A, Dastugue, N, Talmant, P, Bilhou-Nabera, C, Mugneret, F, Lafage-Pochitaloff, M, Mozziconacci, M-J, Andrieu, J, Lai, J-L, Terre, C, Rack, K, Cornillet-Lefebvre, P, Luquet, I, Nadal, N, Nguyen-Khac, F, Perot, C, Van den Akker, J, Fert-Ferrer, S, Cabrol, C, Charrin, C, Tigaud, I, Poirel, H, Vekemans, M, Bernard, O A, and Berger, R
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- 2006
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5. Atypical response to all-trans retinoic acid in a der(5)t(5;17) acute promyelocytic leukemia
- Author
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Mozziconacci, Mj, Liberatore, C, Grignani, Francesco, Sainty, D, Pelicci, Pg, Birg, F, and LAFAGE POCHITALOFF, M.
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PML/RAR ,Retinoic Acid ,leukemia - Published
- 1999
6. In vitro response to all trans Retinoic acid of acute promyelocytic leukemia with non reciprocal PML/RARa or RAR/PML fusion genes
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Mozziconacci, Mj, Liberatore, Concetta, Brunel, V., Grignani, Francesco, Arnoulet, C., Ferrucci, Pf, Fernandez, F., Sainty, D., Pelicci, Pg, Birg, F., and LAFAGE POCHITALOFF, M.
- Subjects
Leukemia ,Retinoic Acid ,PML/RAR - Published
- 1998
7. NUP98–HMGB3: a novel oncogenic fusion.
- Author
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Petit, A, Ragu, C, Della-Valle, V, Mozziconacci, M J, Lafage-Pochitaloff, M, Soler, G, Schluth, C, Radford, I, Ottolenghi, C, Bernard, O A, Penard-Lacronique, V, and Romana, S P
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CANCER ,BONE marrow ,GENES ,LEUKEMIA ,CANCER genes ,CHARTS, diagrams, etc. - Abstract
The article discusses about the NUP98 promiscuou gene. It is involved in chromosomal aberrations with other genes in variety of human hematological malignancies. Study of overexpression in mouse bone marrow indicates that NUP98 induce leukemic transformation. The article reports about the involvement of NUP98 in the therapy related acute myeloblastic leukemia. The article also describes the process of NUP98-HMBG3 fusion. Various charts related to the experiment is presented.
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- 2010
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8. Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRβ-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
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Cauwelier, B., Cavé, H., Gervais, C., Lessard, M., Barin, C., Perot, C., Van den Akker, J., Mugneret, F., Charrin, C., Pagès, M. P., Grégoire, M.-J., Jonveaux, P., Lafage-Pochitaloff, M., Mozzicconacci, M. J., Terré, C., Luquet, I., Cornillet-Lefebvre, P., Laurence, B., Plessis, G., and Lefebvre, C.
- Subjects
CYTOGENETICS ,CELL receptors ,LEUKEMIA ,CARCINOGENESIS ,MOLECULAR genetics ,IN situ hybridization ,BONE marrow ,IMMUNOPHENOTYPING - Abstract
Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRβ) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10. To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs. This revealed TCRβ-HOXA rearrangements in five additional patients, which brings the total to 14 cases in 424 patients (3.3%). Real-time quantitative PCR analysis for HOXA10 gene expression was performed in 170 T-ALL patients and detected HOXA10 overexpression in 25.2% of cases including all the cases with a TCRβ-HOXA rearrangement (8.2%). In contrast, expression of the short HOXA10 transcript, HOXA10b, was almost exclusively found in the TCRβ-HOXA rearranged cases, suggesting a specific role for the HOXA10b short transcript in TCRβ-HOXA-mediated oncogenesis. Other molecular and/or cytogenetic aberrations frequently found in subtypes of T-ALL (SIL-TAL1, CALM-AF10, HOX11, HOX11L2) were not detected in the TCRβ-HOXA rearranged cases except for deletion 9p21 and NOTCH1 activating mutations, which were present in 64 and 67%, respectively. In conclusion, this study defines TCRβ-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.Leukemia (2007) 21, 121–128. doi:10.1038/sj.leu.2404410; published online 12 October 2006 [ABSTRACT FROM AUTHOR]
- Published
- 2007
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9. Report of 34 patients with clonal chromosomal abnormalities in Philadelphia-negative cells during imatinib treatment of Philadelphia-positive chronic myeloid leukemia.
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Terre, C., Eclache, V., Rousselot, P., Imbert, M., Charrin, C., Gervais, C., Mozziconacci, M. J., Maarek, O., Mossafa, H., Auger, N., Dastugue, N., Talmant, P., Van Den Akker, J., Leonard, C., N'Guyen Khac, F., Mugneret, F., Viguié, F., Lafage-Pochitaloff, M., Bastie, J. N., and Roux, G. l.
- Subjects
IMATINIB ,MYELOID leukemia ,PROTEIN-tyrosine kinases ,CHROMOSOMES ,ANTINEOPLASTIC agents ,LEUKEMIA - Abstract
Imatinib mesylate (Gleevec
® ), an inhibitor of the BCR-ABL tyrosine kinase, was introduced recently into the therapy of chronic myeloid leukemia (CML). Several cases of emergence of clonal chromosomal abnormalities after therapy with imatinib have been reported, but their incidence, etiology and prognosis remain to be clarified. We report here a large series of 34 CML patients treated with imatinib who developed Philadelphia (Ph)-negative clones. Among 1001 patients with Ph-positive CML treated with imatinib, 34 (3.4%) developed clonal chromosomal abnormalities in Ph-negative cells. Three patients were treated with imatinib up-front. The most common cytogenetic abnormalities were trisomy 8 and monosomy 7 in twelve and seven patients, respectively. In 15 patients, fluorescent in situ hybridization with specific probes was performed in materials archived before the initiation of imatinib. The Ph-negative clone was related to previous therapy in three patients, and represented a minor pre-existing clone that expanded after the eradication of Ph-positive cells with imatinib in two others. However, in 11 patients, the new clonal chromosomal abnormalities were not detected and imatinib may have had a direct effect. No myelodysplasia was found in our cohort. With a median follow-up of 24 months, one patient showed CML acceleration and two relapsed.Leukemia (2004) 18, 1340-1346. doi:10.1038/sj.leu.2403399 Published online 10 June 2004 [ABSTRACT FROM AUTHOR]- Published
- 2004
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10. Essential of conventional and molecular cytogenetics: application to diagnosis of hematological malignancies
- Author
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Lafage-Pochitaloff, M.
- Published
- 2003
- Full Text
- View/download PDF
11. Atypical response to all-trans retinoic acid in a der(5)t(5;17) acute promyelocytic leukemia.
- Author
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Mozziconacci, M-J, Liberatore, C, Grignani, F, Sainty, D, Pelicci, P G, Birg, F, and Lafage-Pochitaloff, M
- Subjects
TRETINOIN ,LEUKEMIA - Abstract
Typical acute promyelocytic leukemia (APL) is associated with the t(15;17) translocation, expression of a PML/RARA fusion transcript, and responsiveness to all-trans retinoic acid (ATRA). Rare APL cases implicating the RARA but not the PML gene have been reported. Cases with t(11;17)(q23;q21) which fuses the PLZF and RARA genes do not respond to ATRA. In contrast, cases with t(11;17)(q13;q21) and t(5;17)(q35;q21) which fuse RARA with NuMA and NPM, respectively, were reported to be sensitive to ATRA. We described previously an APL case with an unbalanced t(5;17) implicating RARA but neither PML nor PLZF. Here, we show that in this case: (1) the NPM gene is not involved, as demonstrated by RT-PCR and Southern blot; (2) response to ATRA in vitro is atypical, as demonstrated by morphological and functional maturation assays; and (3) PML nuclear bodies are not disrupted, as evidenced by immunofluorescence staining. [ABSTRACT FROM AUTHOR]
- Published
- 1999
- Full Text
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12. Ten novel 11q23 chromosomal partner sites. European 11q23 Workshop participants.
- Author
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Harrison, C J, Cuneo, A, Clark, R, Johansson, B, Lafage-Pochitaloff, M, Mugneret, F, Moorman, A V, and Secker-Walker, L M
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GENES ,LEUKEMIA ,CHROMOSOMES ,MYELODYSPLASTIC syndromes ,PROTEINS ,DNA ,LYMPHOBLASTIC leukemia ,ONCOGENES ,MYELOID leukemia ,CHROMOSOME banding ,KARYOTYPES ,CHROMOSOME abnormalities ,TRANSFERASES ,DNA-binding proteins ,TRANSCRIPTION factors ,ACUTE diseases - Abstract
The MLL gene located at 11q23 has been described as a 'promiscuous' gene due its involvement with a large number of genetic partners. The EU Concerted Action Workshop on 11q23 provided 550 cases for study of which 82 showed abnormalities which did not involve the established translocations or deletion of 11q23. In these 'other' cases, which included inversions and duplications, 11q23 was found to be involved with 25 chromosome partners of which 10 had not been previously reported. These were 1q31, 4p11, 6q13, 8q21, 10q22, 10q25, 11q11, 11q21, 13q34 and 18q23. This study demonstrated the value of the Workshop, in confirming the diversity of chromosomal partner sites involved with 11q23 and in the identification of new partners. [ABSTRACT FROM AUTHOR]
- Published
- 1998
- Full Text
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13. Cytogenetic study of 75 erythroleukemias
- Author
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Lessard, M., Struski, S., Leymarie, V., Flandrin, G., Lafage-Pochitaloff, M., Mozziconacci, M.-J., Talmant, P., Bastard, C., Charrin, C., Baranger, L., Hélias, C., Cornillet-Lefebvre, P., Mugneret, F., Cabrol, C., Pagès, M.-P., Fert-Ferret, D., Nguyen-Khac, F., Quilichini, B., Barin, C., and Berger, R.
- Subjects
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GENETICS , *CELL nuclei , *LEUKEMIA , *CHROMOSOME abnormalities - Abstract
Abstract: Chromosomal abnormalities of erythroleukemia (EL) are often described as complex and unspecific. A retrospective study of 75 EL defined following the WHO classification was performed by the Groupe Francophone de Cytogénétique Hématologique (GFCH) in order to reexamine the cytogenetics of this infrequent leukemia subtype. Clonal chromosomal abnormalities were found in 57 patients (76%), distributed in 4 subgroups according to their ploidy status: pseudodiploid (16%), hypodiploid (47%), hyperdiploid (19%), and 18% mixed cases associating 2 different clones (hypodiploid + hyperdiploid) or (pseudodiploid + hyperdiploid). Complex rearrangements and hypodiploid chromosome number were widely dominant (50%). Partial or entire monosomies represented 56% of abnormalities. Chromosomes 5 and 7 were the most frequently involved (41 and 33 times, respectively), followed by chromosomes 8, 16, and 21 (19 times each). Unbalanced abnormalities were more frequent than balanced. All these kinds of abnormalities were observed in de novo as well as in secondary EL. Four out of 7 cases of “pure erythroid” leukemia were associated with a BCR-ABL fusion. Lastly, no chromosome abnormality specific to EL could be established. However, the large overlap of chromosomal abnormality patterns of EL (pure erythroid form excepted) and refractory anemia with excess of blasts in transformation (RAEB-t) favors the hypothesis of similarities between these 2 hematologic disorders. [Copyright &y& Elsevier]
- Published
- 2005
- Full Text
- View/download PDF
14. Dasatinib and low-intensity chemotherapy in elderly patients with Philadelphia chromosome-positive ALL
- Author
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Magda Alexis, Norbert Ifrah, Laurent Sutton, Bruno Lioure, Patrice Chevallier, Jean-Michel Cayuela, Carlo Gambacorti Passerini, Valérie Robin, André Delannoy, José Fernandes, Françoise Huguet, Oumedaly Reman, Philippe Rousselot, Laure Morisset, Thibaut Leguay, Sandrine Hayette, Anne Banos, Caroline Bonmati, marie Magdelaine Coude, Philippe Agape, Renato Bassan, Xavier Thomas, Sylvie Glaisner, Celia Salanoubat, Josep M. Ribera, Dieter Hoelzer, Anne Bornand, Heike Pfeifer, Oliver G. Ottmann, Eric Jourdan, Marina Lafage-Pochitaloff, Marc Delord, Mathilde Hunault, Christian Berthou, Nicola Gökbuget, Hervé Dombret, Le Collège d'études mondiales/FMSH, Fondation Maison des sciences de l'homme (FMSH), Laboratoire Central d'Anatomie et de Cytologie Pathologiques [Hôpital Edouard Herriot - HCL], Hôpital Edouard Herriot [CHU - HCL], Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], CHU Bordeaux [Bordeaux], Centre d'investigation clinique en cancérologie (CI2C), Centre hospitalier universitaire de Nantes (CHU Nantes), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Centre Hospitalier Régional d'Orléans (CHRO), Lymphocyte B et Auto-immunité (LBAI), Université de Brest (UBO)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Centre Hospitalier Saint Jean de Perpignan, Hôpital d'Argenteuil, Hôpital de Bayonne, CH de la Côte Basque, Institut d'Hématologie de Basse-Normandie (IHBN), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN)-Centre Régional de Lutte contre le Cancer François Baclesse [Caen] (UNICANCER/CRLC), UNICANCER-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-UNICANCER, CHU Strasbourg, Hospices Civils de Lyon (HCL), Assistance Publique - Hôpitaux de Marseille (APHM), Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7), Hôpital Saint-Louis, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Centre de Recherche en Cancérologie de Lyon (CRCL), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Centre Hospitalier Régional d'Orléans (CHR), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO), Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN)-Centre Régional de Lutte contre le Cancer François Baclesse (CRLC François Baclesse ), Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7), Rousselot, P, Coudé, M, Gokbuget, N, Gambacorti Passerini, C, Hayette, S, Cayuela, J, Huguet, F, Leguay, T, Chevallier, P, Salanoubat, C, Bonmati, C, Alexis, M, Hunault, M, Glaisner, S, Agape, P, Berthou, C, Jourdan, E, Fernandes, J, Sutton, L, Banos, A, Reman, O, Lioure, B, Thomas, X, Ifrah, N, Lafage-Pochitaloff, M, Bornand, A, Morisset, L, Robin, V, Pfeifer, H, Delannoy, A, Ribera, J, Bassan, R, Delord, M, Hoelzer, D, Dombret, H, and Ottmann, O
- Subjects
Male ,Oncology ,Survival ,Clinical Trials and Observations ,diagnosis ,medicine.medical_treatment ,Dasatinib ,Fusion Proteins, bcr-abl ,Hematopoietic stem cell transplantation ,Comorbidity ,Biochemistry ,Polymerase Chain Reaction ,Dexamethasone ,0302 clinical medicine ,Maintenance therapy ,Belgium ,Germany ,hemic and lymphatic diseases ,Philadelphia Chromosome ,genetics ,Prospective Studies ,Aged, 80 and over ,Leukemia ,Cytarabine ,Hematopoietic Stem Cell Transplantation ,Hematology ,Middle Aged ,Precursor Cell Lymphoblastic Leukemia-Lymphoma ,Prognosis ,3. Good health ,Italy ,Vincristine ,030220 oncology & carcinogenesis ,Medicine ,Female ,France ,medicine.drug ,Risk ,Adult ,medicine.medical_specialty ,Patients ,Immunology ,Antineoplastic Agents ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,03 medical and health sciences ,Internal medicine ,medicine ,Humans ,Asparaginase ,Dasatinib, TKI, Ph+ ALL ,Protein Kinase Inhibitors ,Molecular Biology ,Aged ,Chemotherapy ,therapy ,business.industry ,Cell Biology ,R1 ,Surgery ,Transplantation ,Imatinib mesylate ,Methotrexate ,Mutation ,business ,Laboratories ,030215 immunology ,transplantation ,Stem Cell Transplantation - Abstract
International audience; Prognosis of Philadelphia-positive (Ph(+)) acute lymphoblastic leukemia (ALL) in the elderly has improved during the imatinib era. We investigated dasatinib, another potent tyrosine kinase inhibitor, in combination with low-intensity chemotherapy. Patients older than age 55 years were included in the European Working Group on Adult ALL (EWALL) study number 01 for Ph(+) ALL (EWALL-PH-01 international study) and were treated with dasatinib 140 mg/day (100 mg/day over 70 years) with intrathecal chemotherapy, vincristine, and dexamethasone during induction. Patients in complete remission continued consolidation with dasatinib, sequentially with cytarabine, asparaginase, and methotrexate for 6 months. Maintenance therapy was dasatinib and vincristine/dexamethasone reinductions for 18 months followed by dasatinib until relapse or death. Seventy-one patients with a median age of 69 years were enrolled; 77% had a high comorbidity score. Complete remission rate was 96% and 65% of patients achieved a 3-log reduction in BCR-ABL1 transcript levels during consolidation. Only 7 patients underwent allogeneic hematopoietic stem cell transplantation. At 5 years, overall survival was 36% and up to 45% taking into account deaths unrelated to disease or treatment as competitors. Thirty-six patients relapsed, 24 were tested for mutation by Sanger sequencing, and 75% were T315I-positive. BCR-ABL1(T315I) was tested by allele-specific oligonucleotide reverse transcription-quantitative polymerase chain reaction in 43 patients and detection was associated with short-term relapses. Ten patients (23%) were positive before any therapy and 8 relapsed, all with this mutation. In conclusion, dasatinib combined with low-intensity chemotherapy was well-tolerated and gave long-term survival in 36% of elderly patients with Ph(+) ALL. Monitoring of BCR-ABL1(T315I) from diagnosis identified patients with at high risk of early relapse and may help to personalize therapy
- Published
- 2016
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