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498 results on '"Delabesse, E."'

1. The KMT2A recombinome of acute leukemias in 2023

Author

Meyer, C., Larghero, P., Almeida Lopes, B., Burmeister, T., Gröger, D., Sutton, R., Venn, N. C., Cazzaniga, G., Corral Abascal, L., Tsaur, G., Fechina, L., Emerenciano, M., Pombo-de-Oliveira, M. S., Lund-Aho, T., Lundán, T., Montonen, M., Juvonen, V., Zuna, J., Trka, J., Ballerini, P., Lapillonne, H., Van der Velden, V. H. J., Sonneveld, E., Delabesse, E., de Matos, R. R. C., Silva, M. L. M., Bomken, S., Katsibardi, K., Keernik, M., Grardel, N., Mason, J., Price, R., Kim, J., Eckert, C., Lo Nigro, L., Bueno, C., Menendez, P., zur Stadt, U., Gameiro, P., Sedék, L., Szczepański, T., Bidet, A., Marcu, V., Shichrur, K., Izraeli, S., Madsen, H. O., Schäfer, B. W., Kubetzko, S., Kim, R., Clappier, E., Trautmann, H., Brüggemann, M., Archer, P., Hancock, J., Alten, J., Möricke, A., Stanulla, M., Lentes, J., Bergmann, A. K., Strehl, S., Köhrer, S., Nebral, K., Dworzak, M. N., Haas, O. A., Arfeuille, C., Caye-Eude, A., Cavé, H., and Marschalek, R.

Published
2023
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3. LMO2-Associated Clonal T Cell Proliferation in Two Patients after Gene Therapy for SCID-X1

Author

Von Kalle, C., Schmidt, M., McCormack, M. P., Wulffraat, N., Leboulch, P., Lim, A., Osborne, C. S., Pawliuk, R., Morillon, E., Sorensen, R., Forster, A., Fraser, P., Cohen, J. I., Alexander, I., Wintergerst, U., Frebourg, T., Aurias, A., Stoppa-Lyonnet, D., Romana, S., Radford-Weiss, I., Gross, F., Valensi, F., Delabesse, E., Macintyre, E., Sigaux, F., Soulier, J., Leiva, L. E., Wissler, M., Prinz, C., Rabbitts, T. H., Le Deist, F., Fischer, A., and Cavazzana-Calvo, M.

Published
2003

4. NUP98 is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis

Author

Struski, S, Lagarde, S, Bories, P, Puiseux, C, Prade, N, Cuccuini, W, Pages, M-P, Bidet, A, Gervais, C, Lafage-Pochitaloff, M, Roche-Lestienne, C, Barin, C, Penther, D, Nadal, N, Radford-Weiss, I, Collonge-Rame, M-A, Gaillard, B, Mugneret, F, Lefebvre, C, Bart-Delabesse, E, Petit, A, Leverger, G, Broccardo, C, Luquet, I, Pasquet, M, and Delabesse, E

Published
2017
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5. Hypodiploidy has unfavorable impact on survival in pediatric acute myeloid leukemia: An I-BFM Study Group collaboration

Author

Hammer, A. S. B., Juul-Dam, K. L., Sandahl, J. D., Abrahamsson, J., Czogala, M., Delabesse, E., Haltrich, I., Jahnukainen, K., Kolb, E. A., Kovacs, G., Leverger, G., Locatelli, Franco, Masetti, R., Noren-Nystro, U., Raimondi, S. C., Rasche, M., Reinhardt, D., Taki, T., Tomizawa, D., Zeller, B., Hasle, H., Kjeldsen, E., Locatelli F. (ORCID:0000-0002-7976-3654), Hammer, A. S. B., Juul-Dam, K. L., Sandahl, J. D., Abrahamsson, J., Czogala, M., Delabesse, E., Haltrich, I., Jahnukainen, K., Kolb, E. A., Kovacs, G., Leverger, G., Locatelli, Franco, Masetti, R., Noren-Nystro, U., Raimondi, S. C., Rasche, M., Reinhardt, D., Taki, T., Tomizawa, D., Zeller, B., Hasle, H., Kjeldsen, E., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

Hypodiploidy, defined as modal numbers (MNs) 45 or lower, has not been independently investigated in pediatric acute myeloid leukemia (AML) but is a well-described high-risk factor in pediatric acute lymphoblastic leukemia. We aimed to characterize and study the prognostic impact of hypodiploidy in pediatric AML. In this retrospective cohort study, we included children below 18 years of age with de novo AML and a hypodiploid karyotype diagnosed from 2000 to 2015 in 14 childhood AML groups from the International Berlin-Frankfurt-Münster (I-BFM) framework. Exclusion criteria comprised constitutional hypodiploidy, monosomy 7, composite karyotype, and t(8;21) with concurring sex chromosome loss. Hypodiploidy occurred in 81 patients (1.3%) with MNs, 45 (n = 66); 44 (n = 10) and 43 (n = 5). The most frequently lost chromosomes were chromosome 9 and sex chromosomes. Five-year event-free survival (EFS) and overall survival (OS) were 34% and 52%, respectively, for the hypodiploid cohort. Children with MN≤44 (n = 15) had inferior EFS (21%) and OS (33%) compared with children with MN = 45 (n = 66; EFS, 37%; OS, 56%). Adjusted hazard ratios (HRs) were 4.9 (P = .001) and 6.1 (P = .003). Monosomal karyotype or monosomy 9 had particular poor OS (43% and 15%, respectively). Allogeneic stem cell transplantation (SCT) in first complete remission (CR1) (n = 18) did not mitigate the unfavorable outcome of hypodiploidy (adjusted HR for OS was 1.5; P = .42). We identified pediatric hypodiploid AML as a rare subgroup with an inferior prognosis even in the patients treated with SCT in CR1.

Published
2023

6. The KMT2A recombinome of acute leukemias in 2023

Author

Meyer, C, Larghero, P, Almeida Lopes, B; https://orcid.org/0000-0003-1072-470X, Burmeister, T; https://orcid.org/0000-0003-4843-2876, Gröger, D, Sutton, R; https://orcid.org/0000-0002-0188-6005, Venn, N C, Cazzaniga, G, Corral Abascal, L, Tsaur, G, Fechina, L, Emerenciano, M; https://orcid.org/0000-0003-2337-8420, Pombo-de-Oliveira, M S; https://orcid.org/0000-0002-1507-004X, Lund-Aho, T, Lundán, T, Montonen, M, Juvonen, V, Zuna, J; https://orcid.org/0000-0002-0887-3709, Trka, J, Ballerini, P, Lapillonne, H, Van der Velden, V H J; https://orcid.org/0000-0001-9457-3763, Sonneveld, E, Delabesse, E, de Matos, R R C; https://orcid.org/0000-0002-8737-1669, Silva, M L M; https://orcid.org/0000-0003-2549-1320, Bomken, S; https://orcid.org/0000-0001-9163-5738, Katsibardi, K, Keernik, M, Schäfer, Beat W; https://orcid.org/0000-0001-5988-2915, et al, Meyer, C, Larghero, P, Almeida Lopes, B; https://orcid.org/0000-0003-1072-470X, Burmeister, T; https://orcid.org/0000-0003-4843-2876, Gröger, D, Sutton, R; https://orcid.org/0000-0002-0188-6005, Venn, N C, Cazzaniga, G, Corral Abascal, L, Tsaur, G, Fechina, L, Emerenciano, M; https://orcid.org/0000-0003-2337-8420, Pombo-de-Oliveira, M S; https://orcid.org/0000-0002-1507-004X, Lund-Aho, T, Lundán, T, Montonen, M, Juvonen, V, Zuna, J; https://orcid.org/0000-0002-0887-3709, Trka, J, Ballerini, P, Lapillonne, H, Van der Velden, V H J; https://orcid.org/0000-0001-9457-3763, Sonneveld, E, Delabesse, E, de Matos, R R C; https://orcid.org/0000-0002-8737-1669, Silva, M L M; https://orcid.org/0000-0003-2549-1320, Bomken, S; https://orcid.org/0000-0001-9163-5738, Katsibardi, K, Keernik, M, Schäfer, Beat W; https://orcid.org/0000-0001-5988-2915, and et al

Abstract

Chromosomal rearrangements of the human KMT2A/MLL gene are associated with de novo as well as therapy-induced infant, pediatric, and adult acute leukemias. Here, we present the data obtained from 3401 acute leukemia patients that have been analyzed between 2003 and 2022. Genomic breakpoints within the KMT2A gene and the involved translocation partner genes (TPGs) and KMT2A-partial tandem duplications (PTDs) were determined. Including the published data from the literature, a total of 107 in-frame KMT2A gene fusions have been identified so far. Further 16 rearrangements were out-of-frame fusions, 18 patients had no partner gene fused to 5'-KMT2A, two patients had a 5'-KMT2A deletion, and one ETV6::RUNX1 patient had an KMT2A insertion at the breakpoint. The seven most frequent TPGs and PTDs account for more than 90% of all recombinations of the KMT2A, 37 occur recurrently and 63 were identified so far only once. This study provides a comprehensive analysis of the KMT2A recombinome in acute leukemia patients. Besides the scientific gain of information, genomic breakpoint sequences of these patients were used to monitor minimal residual disease (MRD). Thus, this work may be directly translated from the bench to the bedside of patients and meet the clinical needs to improve patient survival.

Published
2023

7. Measurable Residual Disease and Fusion Partner Independently Predict Survival and Relapse Risk in Childhood KMT2A -Rearranged Acute Myeloid Leukemia: A Study by the International Berlin-Frankfurt-Münster Study Group

Author

Van Weelderen, R. E., Klein, K., Harrison, C. J., Jiang, Y., Abrahamsson, J., Arad-Cohen, N., Bart-Delabesse, E., Buldini, B., De Moerloose, B., Dworzak, M. N., Elitzur, S., Fernandez Navarro, J. M., Gerbing, R. B., Goemans, B. F., De Groot-Kruseman, H. A., Guest, E., Ha, S. -Y., Hasle, H., Kelaidi, C., Lapillonne, H., Leverger, G., Locatelli, Franco, Masetti, R., Miyamura, T., Noren-Nystrom, U., Polychronopoulou, S., Rasche, M., Rubnitz, J. E., Stary, J., Tierens, A., Tomizawa, D., Zwaan, C. M., Kaspers, G. J. L., Locatelli F. (ORCID:0000-0002-7976-3654), Van Weelderen, R. E., Klein, K., Harrison, C. J., Jiang, Y., Abrahamsson, J., Arad-Cohen, N., Bart-Delabesse, E., Buldini, B., De Moerloose, B., Dworzak, M. N., Elitzur, S., Fernandez Navarro, J. M., Gerbing, R. B., Goemans, B. F., De Groot-Kruseman, H. A., Guest, E., Ha, S. -Y., Hasle, H., Kelaidi, C., Lapillonne, H., Leverger, G., Locatelli, Franco, Masetti, R., Miyamura, T., Noren-Nystrom, U., Polychronopoulou, S., Rasche, M., Rubnitz, J. E., Stary, J., Tierens, A., Tomizawa, D., Zwaan, C. M., Kaspers, G. J. L., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

PURPOSEA previous study by the International Berlin-Frankfurt-Münster Study Group (I-BFM-SG) on childhood KMT2A-rearranged (KMT2A-r) AML demonstrated the prognostic value of the fusion partner. This I-BFM-SG study investigated the value of flow cytometry-based measurable residual disease (flow-MRD) and evaluated the benefit of allogeneic stem-cell transplantation (allo-SCT) in first complete remission (CR1) in this disease.METHODSA total of 1,130 children with KMT2A-r AML, diagnosed between January 2005 and December 2016, were assigned to high-risk (n = 402; 35.6%) or non-high-risk (n = 728; 64.4%) fusion partner-based groups. Flow-MRD levels at both end of induction 1 (EOI1) and 2 (EOI2) were available for 456 patients and were considered negative (<0.1%) or positive (%0.1%). End points were 5-year event-free survival (EFS), cumulative incidence of relapse (CIR), and overall survival (OS).RESULTSThe high-risk group had inferior EFS (30.3% high risk v 54.0% non-high risk; P <.0001), CIR (59.7% v 35.2%; P <.0001), and OS (49.2% v 70.5%; P <.0001). EOI2 MRD negativity was associated with superior EFS (n = 413; 47.6% MRD negativity v n = 43; 16.3% MRD positivity; P <.0001) and OS (n = 413; 66.0% v n = 43; 27.9%; P <.0001), and showed a trend toward lower CIR (n = 392; 46.1% v n = 26; 65.4%; P =.016). Similar results were obtained for patients with EOI2 MRD negativity within both risk groups, except that within the non-high-risk group, CIR was comparable with that of patients with EOI2 MRD positivity. Allo-SCT in CR1 only reduced CIR (hazard ratio, 0.5 [95% CI, 0.4 to 0.8]; P =.00096) within the high-risk group but did not improve OS. In multivariable analyses, EOI2 MRD positivity and high-risk group were independently associated with inferior EFS, CIR, and OS.CONCLUSIONEOI2 flow-MRD is an independent prognostic factor and should be included as risk stratification factor in childhood KMT2A-r AML. Treatment approaches other than allo-SCT in CR1 are nee

Published
2023

9. P421: LOWER VΓ9VΔ2 T CELLS RELATIVE FREQUENCIES PREDICT POORER SURVIVAL IN NEWLY DIAGNOSED ACUTE MYELOID LEUKEMIA

Author

Le Floch, A.-C., primary, Orlanducci, F., additional, Le Roy, A., additional, Hamel, J.-F., additional, Ifrah, N., additional, Cornillet-Lefebvre, P., additional, Delaunay, J., additional, Récher, C., additional, Delabesse, E., additional, Pigneux, A., additional, Béné, M.-C., additional, Vey, N., additional, Chretien, A.-S., additional, and Olive, D., additional

Published
2022
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10. S162: SOMATIC GENETIC LANDSCAPE IN GATA2 DEFICIENCY PATIENTS

Author

Largeaud, L., primary, Collin, M., additional, Monselet, N., additional, Vergez, F., additional, Larcher, L., additional, Hirsch, P., additional, Duployez, N., additional, Bustamante, J., additional, Bellanné-Chantelot, C., additional, Donadieu, J., additional, Sicre de Fontbrune, F., additional, Nolla, M., additional, Fieschi, C., additional, Delhommeau, F., additional, Delabesse, E., additional, and Pasquet, M., additional

Published
2022
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11. P477: PHENOTYPICALLY-DEFINED STAGES OF LEUKEMIA ARREST PREDICT MAIN DRIVER MUTATIONS SUBGROUPS, AND OUTCOME IN ACUTE MYELOID LEUKEMIA

Author

Vergez, F., primary, Largeaud, L., additional, Bertoli, S., additional, Nicolau-Travers, M.-L., additional, Rieu, J.-B., additional, Vergnolle, I., additional, Saland, E., additional, Sarry, A., additional, Tavitian, S., additional, Huguet, F., additional, Picard, M., additional, Vial, J.-P., additional, Lechevalier, N., additional, Bidet, A., additional, Dumas, P.-Y., additional, Pigneux, A., additional, Luquet, I., additional, Mansat-De Mas, V., additional, Delabesse, E., additional, Carroll, M., additional, Danet-Desnoyers, G., additional, Sarry, J.-E., additional, and Recher, C., additional

Published
2022
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12. The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11

Author

Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., Delabesse, E., Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., and Delabesse, E.

Abstract

Item does not contain fulltext

Published
2022

13. Flow cytometry and IG/TCR quantitative PCR for minimal residual disease quantitation in acute lymphoblastic leukemia: a French multicenter prospective study on behalf of the FRALLE, EORTC and GRAALL

Author

Garand, R, Beldjord, K, Cavé, H, Fossat, C, Arnoux, I, Asnafi, V, Bertrand, Y, Boulland, M-L, Brouzes, C, Clappier, E, Delabesse, E, Fest, T, Garnache-Ottou, F, Huguet, F, Jacob, M-C, Kuhlein, E, Marty-Grès, S, Plesa, A, Robillard, N, Roussel, M, Tkaczuk, J, Dombret, H, Macintyre, E, Ifrah, N, Béné, M C, and Baruchel, A

Published
2013
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18. New insights to the MLL recombinome of acute leukemias

Author

Meyer, C, Kowarz, E, Hofmann, J, Renneville, A, Zuna, J, Trka, J, Ben Abdelali, R, Macintyre, E, De Braekeleer, E, De Braekeleer, M, Delabesse, E, de Oliveira, M P, Cavé, H, Clappier, E, van Dongen, J J M, Balgobind, B V, van den Heuvel-Eibrink, M M, Beverloo, H B, Panzer-Grümayer, R, Teigler-Schlegel, A, Harbott, J, Kjeldsen, E, Schnittger, S, Koehl, U, Gruhn, B, Heidenreich, O, Chan, L C, Yip, S F, Krzywinski, M, Eckert, C, Möricke, A, Schrappe, M, Alonso, C N, Schäfer, B W, Krauter, J, Lee, D A, zur Stadt, U, Te Kronnie, G, Sutton, R, Izraeli, S, Trakhtenbrot, L, Lo Nigro, L, Tsaur, G, Fechina, L, Szczepanski, T, Strehl, S, Ilencikova, D, Molkentin, M, Burmeister, T, Dingermann, T, Klingebiel, T, and Marschalek, R

Published
2009
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19. The KMT2Arecombinome of acute leukemias in 2023

Author

Meyer, C., Larghero, P., Almeida Lopes, B., Burmeister, T., Gröger, D., Sutton, R., Venn, N. C., Cazzaniga, G., Corral Abascal, L., Tsaur, G., Fechina, L., Emerenciano, M., Pombo-de-Oliveira, M. S., Lund-Aho, T., Lundán, T., Montonen, M., Juvonen, V., Zuna, J., Trka, J., Ballerini, P., Lapillonne, H., Van der Velden, V. H. J., Sonneveld, E., Delabesse, E., de Matos, R. R. C., Silva, M. L. M., Bomken, S., Katsibardi, K., Keernik, M., Grardel, N., Mason, J., Price, R., Kim, J., Eckert, C., Lo Nigro, L., Bueno, C., Menendez, P., zur Stadt, U., Gameiro, P., Sedék, L., Szczepański, T., Bidet, A., Marcu, V., Shichrur, K., Izraeli, S., Madsen, H. O., Schäfer, B. W., Kubetzko, S., Kim, R., Clappier, E., Trautmann, H., Brüggemann, M., Archer, P., Hancock, J., Alten, J., Möricke, A., Stanulla, M., Lentes, J., Bergmann, A. K., Strehl, S., Köhrer, S., Nebral, K., Dworzak, M. N., Haas, O. A., Arfeuille, C., Caye-Eude, A., Cavé, H., and Marschalek, R.

Abstract

Chromosomal rearrangements of the human KMT2A/MLLgene are associated with de novoas well as therapy-induced infant, pediatric, and adult acute leukemias. Here, we present the data obtained from 3401 acute leukemia patients that have been analyzed between 2003 and 2022. Genomic breakpoints within the KMT2Agene and the involved translocation partner genes (TPGs) and KMT2A-partial tandem duplications (PTDs) were determined. Including the published data from the literature, a total of 107 in-frame KMT2Agene fusions have been identified so far. Further 16 rearrangements were out-of-frame fusions, 18 patients had no partner gene fused to 5’-KMT2A, two patients had a 5’-KMT2Adeletion, and one ETV6::RUNX1patient had an KMT2Ainsertion at the breakpoint. The seven most frequent TPGs and PTDs account for more than 90% of all recombinations of the KMT2A, 37 occur recurrently and 63 were identified so far only once. This study provides a comprehensive analysis of the KMT2Arecombinome in acute leukemia patients. Besides the scientific gain of information, genomic breakpoint sequences of these patients were used to monitor minimal residual disease (MRD). Thus, this work may be directly translated from the bench to the bedside of patients and meet the clinical needs to improve patient survival.

Published
2023
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20. The MLL recombinome of acute leukemias in 2013

Author

Meyer, C, Hofmann, J, Burmeister, T, Gröger, D, Park, T S, Emerenciano, M, Pombo de Oliveira, M, Renneville, A, Villarese, P, Macintyre, E, Cavé, H, Clappier, E, Mass-Malo, K, Zuna, J, Trka, J, De Braekeleer, E, De Braekeleer, M, Oh, S H, Tsaur, G, Fechina, L, van der Velden, V HJ, van Dongen, J JM, Delabesse, E, Binato, R, Silva, M LM, Kustanovich, A, Aleinikova, O, Harris, M H, Lund-Aho, T, Juvonen, V, Heidenreich, O, Vormoor, J, Choi, W WL, Jarosova, M, Kolenova, A, Bueno, C, Menendez, P, Wehner, S, Eckert, C, Talmant, P, Tondeur, S, Lippert, E, Launay, E, Henry, C, Ballerini, P, Lapillone, H, Callanan, M B, Cayuela, J M, Herbaux, C, Cazzaniga, G, Kakadiya, P M, Bohlander, S, Ahlmann, M, Choi, J R, Gameiro, P, Lee, D S, Krauter, J, Cornillet-Lefebvre, P, Te Kronnie, G, Schäfer, B W, Kubetzko, S, Alonso, C N, zur Stadt, U, Sutton, R, Venn, N C, Izraeli, S, Trakhtenbrot, L, Madsen, H O, Archer, P, Hancock, J, Cerveira, N, Teixeira, M R, Lo Nigro, L, Möricke, A, Stanulla, M, Schrappe, M, Sedék, L, Szczepański, T, Zwaan, C M, Coenen, E A, van den Heuvel-Eibrink, M M, Strehl, S, Dworzak, M, Panzer-Grümayer, R, Dingermann, T, Klingebiel, T, and Marschalek, R

Published
2013
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21. The MLL recombinome of acute leukemias in 2017

Author

Meyer, C, Burmeister, T, Gröger, D, Tsaur, G, Fechina, L, Renneville, A, Sutton, R, Venn, N, Emerenciano, M, Pombo-De-Oliveira, M, Barbieri Blunck, C, Almeida Lopes, B, Zuna, J, Trka, J, Ballerini, P, Lapillonne, H, De Braekeleer, M, Cazzaniga, G, Corral Abascal, L, Van Der Velden, V, Delabesse, E, Park, T, Oh, S, Silva, M, Lund-Aho, T, Juvonen, V, Moore, A, Heidenreich, O, Vormoor, J, Zerkalenkova, E, Olshanskaya, Y, Bueno, C, Menendez, P, Teigler-Schlegel, A, Zur Stadt, U, Lentes, J, Göhring, G, Kustanovich, A, Aleinikova, O, Schäfer, B, Kubetzko, S, Madsen, H, Gruhn, B, Duarte, X, Gameiro, P, Lippert, E, Bidet, A, Cayuela, J, Clappier, E, Alonso, C, Zwaan, C, Van Den Heuvel-Eibrink, M, Izraeli, S, Trakhtenbrot, L, Archer, P, Hancock, J, Möricke, A, Alten, J, Schrappe, M, Stanulla, M, Strehl, S, Attarbaschi, A, Dworzak, M, Haas, O, Panzer-Grümayer, R, Sedék, L, Szczepa, T, Caye, A, Suarez, L, Cavé, H, Marschalek, R, Meyer, C., Burmeister, T., Gröger, D., Tsaur, G., Fechina, L., Renneville, A., Sutton, R., Venn, N. C., Emerenciano, M., Pombo-De-Oliveira, M. S., Barbieri Blunck, C., Almeida Lopes, B., Zuna, J., Trka, J., Ballerini, P., Lapillonne, H., De Braekeleer, M., Cazzaniga, G., Corral Abascal, L., Van Der Velden, V. H. J., Delabesse, E., Park, T. S., Oh, S. H., Silva, M. L. M., Lund-Aho, T., Juvonen, V., Moore, A. S., Heidenreich, O., Vormoor, J., Zerkalenkova, E., Olshanskaya, Y., Bueno, C., Menendez, P., Teigler-Schlegel, A., Zur Stadt, U., Lentes, J., Göhring, G., Kustanovich, A., Aleinikova, O., Schäfer, B. W., Kubetzko, S., Madsen, H. O., Gruhn, B., Duarte, X., Gameiro, P., Lippert, E., Bidet, A., Cayuela, J. M., Clappier, E., Alonso, C. N., Zwaan, C. M., Van Den Heuvel-Eibrink, M. M., Izraeli, S., Trakhtenbrot, L., Archer, P., Hancock, J., Möricke, A., Alten, J., Schrappe, M., Stanulla, M., Strehl, S., Attarbaschi, A., Dworzak, M., Haas, O. A., Panzer-Grümayer, R., Sedék, L., Szczepa, T., Caye, A., Suarez, L., Cavé, H., Marschalek, R., Meyer, C, Burmeister, T, Gröger, D, Tsaur, G, Fechina, L, Renneville, A, Sutton, R, Venn, N, Emerenciano, M, Pombo-De-Oliveira, M, Barbieri Blunck, C, Almeida Lopes, B, Zuna, J, Trka, J, Ballerini, P, Lapillonne, H, De Braekeleer, M, Cazzaniga, G, Corral Abascal, L, Van Der Velden, V, Delabesse, E, Park, T, Oh, S, Silva, M, Lund-Aho, T, Juvonen, V, Moore, A, Heidenreich, O, Vormoor, J, Zerkalenkova, E, Olshanskaya, Y, Bueno, C, Menendez, P, Teigler-Schlegel, A, Zur Stadt, U, Lentes, J, Göhring, G, Kustanovich, A, Aleinikova, O, Schäfer, B, Kubetzko, S, Madsen, H, Gruhn, B, Duarte, X, Gameiro, P, Lippert, E, Bidet, A, Cayuela, J, Clappier, E, Alonso, C, Zwaan, C, Van Den Heuvel-Eibrink, M, Izraeli, S, Trakhtenbrot, L, Archer, P, Hancock, J, Möricke, A, Alten, J, Schrappe, M, Stanulla, M, Strehl, S, Attarbaschi, A, Dworzak, M, Haas, O, Panzer-Grümayer, R, Sedék, L, Szczepa, T, Caye, A, Suarez, L, Cavé, H, Marschalek, R, Meyer, C., Burmeister, T., Gröger, D., Tsaur, G., Fechina, L., Renneville, A., Sutton, R., Venn, N. C., Emerenciano, M., Pombo-De-Oliveira, M. S., Barbieri Blunck, C., Almeida Lopes, B., Zuna, J., Trka, J., Ballerini, P., Lapillonne, H., De Braekeleer, M., Cazzaniga, G., Corral Abascal, L., Van Der Velden, V. H. J., Delabesse, E., Park, T. S., Oh, S. H., Silva, M. L. M., Lund-Aho, T., Juvonen, V., Moore, A. S., Heidenreich, O., Vormoor, J., Zerkalenkova, E., Olshanskaya, Y., Bueno, C., Menendez, P., Teigler-Schlegel, A., Zur Stadt, U., Lentes, J., Göhring, G., Kustanovich, A., Aleinikova, O., Schäfer, B. W., Kubetzko, S., Madsen, H. O., Gruhn, B., Duarte, X., Gameiro, P., Lippert, E., Bidet, A., Cayuela, J. M., Clappier, E., Alonso, C. N., Zwaan, C. M., Van Den Heuvel-Eibrink, M. M., Izraeli, S., Trakhtenbrot, L., Archer, P., Hancock, J., Möricke, A., Alten, J., Schrappe, M., Stanulla, M., Strehl, S., Attarbaschi, A., Dworzak, M., Haas, O. A., Panzer-Grümayer, R., Sedék, L., Szczepa, T., Caye, A., Suarez, L., Cavé, H., and Marschalek, R.

Abstract

Chromosomal rearrangements of the human MLL/KMT2A gene are associated with infant, pediatric, adult and therapy-induced acute leukemias. Here we present the data obtained from 2345 acute leukemia patients. Genomic breakpoints within the MLL gene and the involved translocation partner genes (TPGs) were determined and 11 novel TPGs were identified. Thus, a total of 135 different MLL rearrangements have been identified so far, of which 94 TPGs are now characterized at the molecular level. In all, 35 out of these 94 TPGs occur recurrently, but only 9 specific gene fusions account for more than 90% of all illegitimate recombinations of the MLL gene. We observed an age-dependent breakpoint shift with breakpoints localizing within MLL intron 11 associated with acute lymphoblastic leukemia and younger patients, while breakpoints in MLL intron 9 predominate in AML or older patients. The molecular characterization of MLL breakpoints suggests different etiologies in the different age groups and allows the correlation of functional domains of the MLL gene with clinical outcome. This study provides a comprehensive analysis of the MLL recombinome in acute leukemia and demonstrates that the establishment of patient-specific chromosomal fusion sites allows the design of specific PCR primers for minimal residual disease analyses for all patients

Published
2018

23. L’ajout de la lomustine bénéficie aux leucémies myéloïdes aiguës du sujet âgé avec cytogénétique non-défavorable et d’un profil moléculaire à haut risque de l’European Leukemia Net 2017

Author

Largeaud, L., Cornillet-Lefebvre, P., Hamel, J.F., Dumas, P.Y., Prade, N., Dufrechou, S., Plenecassagnes, J., Luquet, I., Blanchet, O., Banos, A., Bene, M.C., Bernard, M., Bertoli, S., Bonmati, C., FORNECKER, L.M., Guièze, R., Hicheri, Y., Hunault-Berger, M., Ianotto, J.C., Jourdan, E., Ojeda-Uribe, M., Peterlin, P., Vey, N., Zerazhi, H., Mineur, A., Cahn, J.Y., Ifrah, N., Récher, C., Pigneux, A., Delabesse, E., Role of intra-Clonal Heterogeneity and Leukemic environment in ThErapy Resistance of chronic leukemias (CHELTER), and Université Clermont Auvergne [2017-2020] (UCA [2017-2020])

Subjects
[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology
Abstract

07-03; International audience

Published
2020

24. Prospective multicentric molecular study for poor prognosis fusion transcripts at diagnosis in adult B-lineage ALL patients: the LALA 94 experience

Author

Picard, C, Hayette, S, Bilhou-Nabera, C, Cayuela, J M, Delabesse, E, Frenoy, N, Preudhomme, C, Dupont, M, Bastard, C, Bories, D, Vaerman, J L, Davi, F, Dastugue, N, Raynaud, S, Lafage, M, Deschaseaux, F, Fest, T, Gaub, M P, Lhéritier, V, Thomas, X, Charrin, C, Boucheix, C, Dombret, H, MacIntyre, E, Fière, D, and Gabert, J

Published
2006
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25. Imatinib and methylprednisolone alternated with chemotherapy improve the outcome of elderly patients with Philadelphia-positive acute lymphoblastic leukemia: results of the GRAALL AFR09 study

Author

Delannoy, A, Delabesse, E, Lhéritier, V, Castaigne, S, Rigal-Huguet, F, Raffoux, E, Garban, F, Legrand, O, Bologna, S, Dubruille, V, Turlure, P, Reman, O, Delain, M, Isnard, F, Coso, D, Raby, P, Buzyn, A, Caillères, S, Darre, S, Fohrer, C, Sonet, A, Bilhou-Nabera, C, Béné, M-C, Dombret, H, Berthaud, P, and Thomas, X

Published
2006
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27. The MLL recombinome of acute leukemias

Author

Meyer, C, Schneider, B, Jakob, S, Strehl, S, Attarbaschi, A, Schnittger, S, Schoch, C, Jansen, M W J C, van Dongen, J J M, den Boer, M L, Pieters, R, Ennas, M-G, Angelucci, E, Koehl, U, Greil, J, Griesinger, F, zur Stadt, U, Eckert, C, Szczepański, T, Niggli, F K, Schäfer, B W, Kempski, H, Brady, H J M, Zuna, J, Trka, J, Nigro, L L, Biondi, A, Delabesse, E, Macintyre, E, Stanulla, M, Schrappe, M, Haas, O A, Burmeister, T, Dingermann, T, Klingebiel, T, and Marschalek, R

Published
2006
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29. Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-cell Leukemia

Author

Laurent, A.P., Siret, A., Ignacimouttou, C., Panchal, K., Diop, M., Jenni, S., Tsai, Y.C., Roos-Weil, D., Aid, Z., Prade, N., Lagarde, S., Plassard, D., Pierron, G., Daudigeos, E., Lecluse, Y., Droin, N., Bornhauser, B.C., Cheung, Laurence, Crispino, J.D., Gaudry, M., Bernard, O.A., Macintyre, E., Barin Bonnigal, C., Kotecha, Rishi, Geoerger, B., Ballerini, P., Bourquin, J.P., Delabesse, E., Mercher, T., Malinge, S., Laurent, A.P., Siret, A., Ignacimouttou, C., Panchal, K., Diop, M., Jenni, S., Tsai, Y.C., Roos-Weil, D., Aid, Z., Prade, N., Lagarde, S., Plassard, D., Pierron, G., Daudigeos, E., Lecluse, Y., Droin, N., Bornhauser, B.C., Cheung, Laurence, Crispino, J.D., Gaudry, M., Bernard, O.A., Macintyre, E., Barin Bonnigal, C., Kotecha, Rishi, Geoerger, B., Ballerini, P., Bourquin, J.P., Delabesse, E., Mercher, T., and Malinge, S.

Abstract

©2020 American Association for Cancer Research. PURPOSE: Children with Down syndrome (constitutive trisomy 21) that develop acute lymphoblastic leukemia (DS-ALL) have a 3-fold increased likelihood of treatment-related mortality coupled with a higher cumulative incidence of relapse, compared with other children with B-cell acute lymphoblastic leukemia (B-ALL). This highlights the lack of suitable treatment for Down syndrome children with B-ALL. EXPERIMENTAL DESIGN: To facilitate the translation of new therapeutic agents into clinical trials, we built the first preclinical cohort of patient-derived xenograft (PDX) models of DS-ALL, comprehensively characterized at the genetic and transcriptomic levels, and have proven its suitability for preclinical studies by assessing the efficacy of drug combination between the MEK inhibitor trametinib and conventional chemotherapy agents. RESULTS: Whole-exome and RNA-sequencing experiments revealed a high incidence of somatic alterations leading to RAS/MAPK pathway activation in our cohort of DS-ALL, as well as in other pediatric B-ALL presenting somatic gain of the chromosome 21 (B-ALL+21). In murine and human B-cell precursors, activated KRASG12D functionally cooperates with trisomy 21 to deregulate transcriptional networks that promote increased proliferation and self renewal, as well as B-cell differentiation blockade. Moreover, we revealed that inhibition of RAS/MAPK pathway activation using the MEK1/2 inhibitor trametinib decreased leukemia burden in several PDX models of B-ALL+21, and enhanced survival of DS-ALL PDX in combination with conventional chemotherapy agents such as vincristine. CONCLUSIONS: Altogether, using novel and suitable PDX models, this study indicates that RAS/MAPK pathway inhibition represents a promising strategy to improve the outcome of Down syndrome children with B-cell precursor leukemia.

Published
2020

32. La tryptase médullaire, un nouveau critère diagnostique de l’atteinte systémique de la mastocytose : étude multicentrique prospective

Author

Bulai Livideanu, C., primary, Lepage, B., additional, Apoil, P.A., additional, Delabesse, E., additional, Freire Severino, M., additional, Laurent, C., additional, Evrard, S., additional, Tournier, E., additional, Degboé, Y., additional, Mailhol, C., additional, Jendoubi, F., additional, Polomat, K., additional, Rossignol, J., additional, Hermine, O., additional, Barete, S., additional, Beylot-Barry, M., additional, Damaj, G.L., additional, and Paul, C., additional

Published
2020
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35. Design and standardization of PCR primers and protocols for detection of clonal immunoglobulin and T-cell receptor gene recombinations in suspect lymphoproliferations: Report of the BIOMED-2 Concerted Action BMH4-CT98-3936

Author

van Dongen, J J M, Langerak, A W, Brüggemann, M, Evans, P A S, Hummel, M, Lavender, F L, Delabesse, E, Davi, F, Schuuring, E, García-Sanz, R, van Krieken, J H J M, Droese, J, González, D, Bastard, C, White, H E, Spaargaren, M, González, M, Parreira, A, Smith, J L, Morgan, G J, Kneba, M, and Macintyre, E A

Published
2003
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37. Sequential chemotherapy by CHOP and DHAP regimens followed by high-dose therapy with stem cell transplantation induces a high rate of complete response and improves event-free survival in mantle cell lymphoma: a prospective study

Author

Lefrère, F, Delmer, A, Suzan, F, Levy, V, Belanger, C, Djabarri, M, Arnulf, B, Damaj, G, Maillard, N, Ribrag, V, Janvier, M, Sebban, C, Casasnovas, R-O, Bouabdallah, R, Dreyfus, F, Verkarre, V, Delabesse, E, Valensi, F, McIntyre, E, Brousse, N, Varet, B, and Hermine, O

Published
2002
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38. LMO2-associated clonal T cell proliferation in two patients after gene therapy for SCID-X1

Author

Hacein-Bey-Abina, S., Von Kalle, C., Schmidt, M., McCormack, M.P., Wulffraat, N., Leboulch, P., Lim, A., Osborne, C.S., Pawliuk, R., Morillon, E., Sorensen, R., Forster, A., Fraser, P., Cohen, J.I., de Saint Basile, G., Alexander, I., Wintergerst, U., Frebourg, T., Aurias, A., Stoppa-Lyonnet, D., Romana, S., Radford-Weiss, I., Gross, F., Valensi, F., Delabesse, E., Macintyre, E., Sigaux, F., Soulier, J., Leiva, L.E., Wissler, M., Prinz, C., Rabbitts, T.H., Le Deist, F., Fischer, A., and Cavazzana-Calvo, M.

Subjects
Physiological aspects, Complications and side effects, Research, Gene therapy -- Research -- Physiological aspects, Retroviruses -- Research -- Physiological aspects
Abstract

Ex vivo retrovirus-mediated gene transfer into hematopoietic progenitor cells has been shown to be an efficient strategy to correct inherited diseases of the lymphohematopoietic system, provided that a strong selective [...], We have previously shown correction of X-linked severe combined immunodeficiency [SCID-X1, also known as γ chain (γc) deficiency] in 9 out of 10 patients by retrovirus-mediated γc gene transfer into autologous CD34 bone marrow cells. However, almost 3 years after gene therapy, uncontrolled exponential clonal proliferation of mature T cells (with γδ+ or αβ+ T cell receptors) has occurred in the two youngest patients. Both patients' clones showed retrovirus vector integration in proximity to the LMO2 proto-oncogene promoter, leading to aberrant transcription and expression of LMO2. Thus, retrovirus vector insertion can trigger deregulated premalignant cell proliferation with unexpected frequency, most likely driven by retrovirus enhancer activity on the LMO2 gene promoter.

Published
2003

41. Standardized RT-PCR analysis of fusion gene transcripts from chromosome aberrations in acute leukemia for detection of minimal residual disease: Report of the BIOMED-1 Concerted Action: Investigation of minimal residual disease in acute leukemia

Author

van Dongen, JJM, Macintyre, EA, Gabert, JA, Delabesse, E, Rossi, V, Saglio, G, Gottardi, E, Rambaldi, A, Dotti, G, Griesinger, F, Parreira, A, Gameiro, P, Diáz, M González, Malec, M, Langerak, AW, San Miguel, JF, and Biondi, A

Published
1999
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47. Ontogenic changes in hematopoietic hierarchy determine pediatric specificity and disease phenotype in fusion oncogene– driven myeloid leukemia

Author

Lopez, C. K., Noguera, E., Stavropoulou, V., Robert, E., Aid, Z., Ballerini, P., Bilhou-Nabera, C., Lapillonne, H., Boudia, F., Thirant, C., Fagnan, A., Arcangeli, M. -L., Kinston, S. J., Diop, M., Job, B., Lecluse, Y., Brunet, E., Babin, L., Villeval, J. L., Delabesse, E., Peters, A. H. F. M., Vainchenker, W., Gaudry, M., Masetti, R., Locatelli, Franco, Malinge, S., Nerlov, C., Droin, N., Lobry, C., Godin, I., Bernard, O. A., Gottgens, B., Petit, A., Pflumio, F., Schwaller, J., Mercher, T., Locatelli F. (ORCID:0000-0002-7976-3654), Lopez, C. K., Noguera, E., Stavropoulou, V., Robert, E., Aid, Z., Ballerini, P., Bilhou-Nabera, C., Lapillonne, H., Boudia, F., Thirant, C., Fagnan, A., Arcangeli, M. -L., Kinston, S. J., Diop, M., Job, B., Lecluse, Y., Brunet, E., Babin, L., Villeval, J. L., Delabesse, E., Peters, A. H. F. M., Vainchenker, W., Gaudry, M., Masetti, R., Locatelli, Franco, Malinge, S., Nerlov, C., Droin, N., Lobry, C., Godin, I., Bernard, O. A., Gottgens, B., Petit, A., Pflumio, F., Schwaller, J., Mercher, T., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

Fusion oncogenes are prevalent in several pediatric cancers, yet little is known about the specific associations between age and phenotype. We observed that fusion oncogenes, such as ETO2–GLIS2, are associated with acute megakaryoblastic or other myeloid leukemia subtypes in an age-dependent manner. Analysis of a novel inducible transgenic mouse model showed that ETO2–GLIS2 expression in fetal hematopoietic stem cells induced rapid megakaryoblastic leukemia whereas expression in adult bone marrow hematopoietic stem cells resulted in a shift toward myeloid transformation with a strikingly delayed in vivo leukemogenic potential. Chromatin accessibility and single-cell transcriptome analyses indicate ontogeny-dependent intrinsic and ETO2–GLIS2-induced differences in the activities of key transcription factors, including ERG, SPI1, GATA1, and CEBPA. Importantly, switching off the fusion oncogene restored terminal differentiation of the leukemic blasts. Together, these data show that aggressiveness and phenotypes in pediatric acute myeloid leukemia result from an ontogeny-related differential susceptibility to transformation by fusion oncogenes. SIGNIFICANCE: This work demonstrates that the clinical phenotype of pediatric acute myeloid leukemia is determined by ontogeny-dependent susceptibility for transformation by oncogenic fusion genes. The phenotype is maintained by potentially reversible alteration of key transcription factors, indicating that targeting of the fusions may overcome the differentiation blockage and revert the leukemic state.

Published
2019

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