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20 results on '"Sarry, J. E."'

1. High mTORC1 activity drives glycolysis addiction and sensitivity to G6PD inhibition in acute myeloid leukemia cells

Author

Poulain, L, Sujobert, P, Zylbersztejn, F, Barreau, S, Stuani, L, Lambert, M, Palama, T L, Chesnais, V, Birsen, R, Vergez, F, Farge, T, Chenevier-Gobeaux, C, Fraisse, M, Bouillaud, F, Debeissat, C, Herault, O, Récher, C, Lacombe, C, Fontenay, M, Mayeux, P, Maciel, T T, Portais, J-C, Sarry, J-E, Tamburini, J, Bouscary, D, and Chapuis, N

Published
2017
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2. 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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7. Oncogenic FLT3-ITD supports autophagy via ATF4 in acute myeloid leukemia

Author

Heydt, Q, Larrue, C., Saland, E, Bertoli, S., Sarry, J-E, Besson, A., Manenti, S., Joffre, C, Mansat-De Mas, V, Cités, Territoires, Environnement et Sociétés (CITERES), Université de Tours-Centre National de la Recherche Scientifique (CNRS), Politecnico di Milano [Milan] (POLIMI), Centre de Recherches en Cancérologie de Toulouse (CRCT), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Physiopathologie Toulouse Purpan ex IFR 30 et IFR 150 (CPTP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université de Tours (UT), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Physiopathologie Toulouse Purpan (CPTP), and Centre National de la Recherche Scientifique (CNRS)-Université de Tours

Subjects
[SDV]Life Sciences [q-bio], hemic and immune systems, Mice, SCID, Activating Transcription Factor 4, Xenograft Model Antitumor Assays, Leukemia, Myeloid, Acute, Mice, fluids and secretions, fms-Like Tyrosine Kinase 3, Drug Resistance, Neoplasm, Mice, Inbred NOD, Tandem Repeat Sequences, hemic and lymphatic diseases, Mutation, embryonic structures, Autophagy, Biomarkers, Tumor, Tumor Cells, Cultured, Animals, Humans, Original Article, Protein Kinase Inhibitors, Cell Proliferation
Abstract

International audience; In acute myeloid leukemia (AML), internal tandem duplication mutations in the FLT3 tyrosine kinase receptor (FLT3-ITD) account for up to 25% of cases and are associated with a poor outcome. In order to better target this AML subtype, a comprehensive view of how FLT3-ITD impacts AML cell biology is required. Here, we found that FLT3-ITD expression increased basal autophagy in AML cells, and that both pharmacological and genetic inhibition of the receptor reduced autophagy in primary AML samples and cell lines. Conditional expression of shRNAs against key autophagy proteins demonstrated that autophagy is required for AML cell proliferation in vitro and for leukemic cells survival in a mouse model of xenograft. Importantly, autophagy inhibition also overcame FLT3 inhibitor resistance both in vitro and in vivo. The transcription factor ATF4 was identified as an essential actor of FLT3-ITD-induced autophagy. Cellular levels of ATF4 were highly dependent on FLT3-ITD activity, and downregulation of ATF4 inhibited autophagy-dependent AML cell proliferation and improved overall mouse survival similarly to autophagy inhibition. These results suggest that targeting autophagy or ATF4 in patients expressing FLT3 mutations may represent a novel promising and innovative therapeutic strategy for AML.

Published
2018

9. RSK2 is a new Pim2 target with pro-survival functions in FLT3-ITD-positive acute myeloid leukemia

Author

Hospital, M-A, primary, Jacquel, A, additional, Mazed, F, additional, Saland, E, additional, Larrue, C, additional, Mondesir, J, additional, Birsen, R, additional, Green, A S, additional, Lambert, M, additional, Sujobert, P, additional, Gautier, E-F, additional, Salnot, V, additional, Le Gall, M, additional, Decroocq, J, additional, Poulain, L, additional, Jacque, N, additional, Fontenay, M, additional, Kosmider, O, additional, Récher, C, additional, Auberger, P, additional, Mayeux, P, additional, Bouscary, D, additional, Sarry, J-E, additional, and Tamburini, J, additional

Published
2017
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11. Bcl-2 protein family expression pattern determines synergistic pro-apoptotic effects of BH3 mimetics with hemisynthetic cardiac glycoside UNBS1450 in acute myeloid leukemia

Author

Cerella, C, primary, Gaigneaux, A, additional, Mazumder, A, additional, Lee, J-Y, additional, Saland, E, additional, Radogna, F, additional, Farge, T, additional, Vergez, F, additional, Récher, C, additional, Sarry, J-E, additional, Kim, K-W, additional, Shin, H Y, additional, Dicato, M, additional, and Diederich, M, additional

Published
2016
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13. A robust and rapid xenograft model to assess efficacy of chemotherapeutic agents for human acute myeloid leukemia

Author

Saland, E, Boutzen, H, Castellano, R, Pouyet, L, Griessinger, E, Larrue, C, de Toni, F, Scotland, S, David, Mathieu, Danet-Desnoyers, G, Vergez, F, Barreira, Y, Collette, Yves, Récher, C, Sarry, J-E, Centre de Recherches en Cancérologie de Toulouse (CRCT), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), IUT de Tarbes, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Centre de Recherche en Cancérologie de Marseille (CRCM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Medicine, Perelman School of Medicine, University of Pennsylvania [Philadelphia]-University of Pennsylvania [Philadelphia], Service d'Expérimentation Animale, UMS006, CHU Toulouse [Toulouse], Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT)-Université de Toulouse (UT), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), University of Pennsylvania-University of Pennsylvania, Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), and HAL AMU, Administrateur

Subjects
BUSULFAN, ENGRAFTMENT, [SDV.CAN] Life Sciences [q-bio]/Cancer, NOD/SCID MICE, TRANSPLANTATION, hemic and lymphatic diseases, IMMUNODEFICIENT MICE, CELLS, [SDV.CAN]Life Sciences [q-bio]/Cancer, HEMATOPOIESIS, neoplasms, IRRADIATION
Abstract

International audience; Relevant preclinical mouse models are crucial to screen new therapeutic agents for acute myeloid leukemia (AML). Current in vivo models based on the use of patient samples are not easy to establish and manipulate in the laboratory. Our objective was to develop robust xenograft models of human AML using well-characterized cell lines as a more accessible and faster alternative to those incorporating the use of patient-derived AML cells. Five widely used AML cell lines representing various AML subtypes were transplanted and expanded into highly immunodeficient non-obese diabetic/LtSz-severe combined immunodeficiency IL2R gamma(null)(c) mice (for example, cell line-derived xenografts). We show here that bone marrow sublethal conditioning with busulfan or irradiation has equal efficiency for the xenotransplantation of AML cell lines. Although higher number of injected AML cells did not change tumor engraftment in bone marrow and spleen, it significantly reduced the overall survival in mice for all tested AML cell lines. On the basis of AML cell characteristics, these models also exhibited a broad range of overall mouse survival, engraftment, tissue infiltration and aggressiveness. Thus, we have established a robust, rapid and straightforward in vivo model based on engraftment behavior of AML cell lines, all vital prerequisites for testing new therapeutic agents in preclinical studies.

Published
2015

14. RSK2 is a new Pim2 target with pro-survival functions in FLT3-ITD-positive acute myeloid leukemia

Author

Hospital, M-A, Jacquel, A, Mazed, F, Saland, E, Larrue, C, Mondesir, J, Birsen, R, Green, A S, Lambert, M, Sujobert, P, Gautier, E-F, Salnot, V, Le Gall, M, Decroocq, J, Poulain, L, Jacque, N, Fontenay, M, Kosmider, O, Récher, C, Auberger, P, Mayeux, P, Bouscary, D, Sarry, J-E, and Tamburini, J

Abstract

Acute myeloid leukemia (AML) with the FLT3 internal tandem duplication (FLT3-ITD AML) accounts for 20–30% of AML cases. This subtype usually responds poorly to conventional therapies, and might become resistant to FLT3 tyrosine kinase inhibitors (TKIs) due to molecular bypass mechanisms. New therapeutic strategies focusing on resistance mechanisms are therefore urgently needed. Pim kinases are FLT3-ITD oncogenic targets that have been implicated in FLT3 TKI resistance. However, their precise biological function downstream of FLT3-ITD requires further investigation. We performed high-throughput transcriptomic and proteomic analyses in Pim2-depleted FLT3-ITD AML cells and found that Pim2 predominantly controlled apoptosis through Bax expression and mitochondria disruption. We identified ribosomal protein S6 kinase A3 (RSK2), a 90?kDa serine/threonine kinase involved in the mitogen-activated protein kinase cascade encoded by the RPS6KA3 gene, as a novel Pim2 target. Ectopic expression of an RPS6KA3 allele rescued the viability of Pim2-depleted cells, supporting the involvement of RSK2 in AML cell survival downstream of Pim2. Finally, we showed that RPS6KA3 knockdown reduced the propagation of human AML cells in vivo in mice. Our results point to RSK2 as a novel Pim2 target with translational therapeutic potential in FLT3-ITD AML.

Published
2018
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16. High levels of CD34+CD38low/-CD123+ blasts are predictive of an adverse outcome in acute myeloid leukemia: a Groupe Ouest-Est des Leucemies Aigues et Maladies du Sang (GOELAMS) study

Author

Vergez, F., primary, Green, A. S., additional, Tamburini, J., additional, Sarry, J.-E., additional, Gaillard, B., additional, Cornillet-Lefebvre, P., additional, Pannetier, M., additional, Neyret, A., additional, Chapuis, N., additional, Ifrah, N., additional, Dreyfus, F., additional, Manenti, S., additional, Demur, C., additional, Delabesse, E., additional, Lacombe, C., additional, Mayeux, P., additional, Bouscary, D., additional, Recher, C., additional, and Bardet, V., additional

Published
2011
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19. Oncogenic FLT3-ITD supports autophagy via ATF4 in acute myeloid leukemia.

Author

Heydt Q, Larrue C, Saland E, Bertoli S, Sarry JE, Besson A, Manenti S, Joffre C, and Mansat-De Mas V

Subjects
Activating Transcription Factor 4 genetics, Animals, Biomarkers, Tumor genetics, Cell Proliferation, Humans, Leukemia, Myeloid, Acute drug therapy, Leukemia, Myeloid, Acute genetics, Leukemia, Myeloid, Acute metabolism, Mice, Mice, Inbred NOD, Mice, SCID, Mutation, Protein Kinase Inhibitors pharmacology, Tandem Repeat Sequences, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, fms-Like Tyrosine Kinase 3 genetics, Activating Transcription Factor 4 metabolism, Autophagy, Biomarkers, Tumor metabolism, Drug Resistance, Neoplasm, Leukemia, Myeloid, Acute pathology, fms-Like Tyrosine Kinase 3 metabolism
Abstract

In acute myeloid leukemia (AML), internal tandem duplication mutations in the FLT3 tyrosine kinase receptor (FLT3-ITD) account for up to 25% of cases and are associated with a poor outcome. In order to better target this AML subtype, a comprehensive view of how FLT3-ITD impacts AML cell biology is required. Here, we found that FLT3-ITD expression increased basal autophagy in AML cells, and that both pharmacological and genetic inhibition of the receptor reduced autophagy in primary AML samples and cell lines. Conditional expression of shRNAs against key autophagy proteins demonstrated that autophagy is required for AML cell proliferation in vitro and for leukemic cells survival in a mouse model of xenograft. Importantly, autophagy inhibition also overcame FLT3 inhibitor resistance both in vitro and in vivo. The transcription factor ATF4 was identified as an essential actor of FLT3-ITD-induced autophagy. Cellular levels of ATF4 were highly dependent on FLT3-ITD activity, and downregulation of ATF4 inhibited autophagy-dependent AML cell proliferation and improved overall mouse survival similarly to autophagy inhibition. These results suggest that targeting autophagy or ATF4 in patients expressing FLT3 mutations may represent a novel promising and innovative therapeutic strategy for AML.

Published
2018
Full Text
View/download PDF

20. A robust and rapid xenograft model to assess efficacy of chemotherapeutic agents for human acute myeloid leukemia.

Author

Saland E, Boutzen H, Castellano R, Pouyet L, Griessinger E, Larrue C, de Toni F, Scotland S, David M, Danet-Desnoyers G, Vergez F, Barreira Y, Collette Y, Récher C, and Sarry JE

Subjects
Animals, Antineoplastic Agents adverse effects, Bone Marrow Cells drug effects, Cell Line, Tumor, Humans, Leukemia, Myeloid, Acute genetics, Leukemia, Myeloid, Acute pathology, Mice, Antineoplastic Agents administration & dosage, Leukemia, Myeloid, Acute drug therapy, Xenograft Model Antitumor Assays methods
Abstract

Relevant preclinical mouse models are crucial to screen new therapeutic agents for acute myeloid leukemia (AML). Current in vivo models based on the use of patient samples are not easy to establish and manipulate in the laboratory. Our objective was to develop robust xenograft models of human AML using well-characterized cell lines as a more accessible and faster alternative to those incorporating the use of patient-derived AML cells. Five widely used AML cell lines representing various AML subtypes were transplanted and expanded into highly immunodeficient non-obese diabetic/LtSz-severe combined immunodeficiency IL2Rγc(null) mice (for example, cell line-derived xenografts). We show here that bone marrow sublethal conditioning with busulfan or irradiation has equal efficiency for the xenotransplantation of AML cell lines. Although higher number of injected AML cells did not change tumor engraftment in bone marrow and spleen, it significantly reduced the overall survival in mice for all tested AML cell lines. On the basis of AML cell characteristics, these models also exhibited a broad range of overall mouse survival, engraftment, tissue infiltration and aggressiveness. Thus, we have established a robust, rapid and straightforward in vivo model based on engraftment behavior of AML cell lines, all vital prerequisites for testing new therapeutic agents in preclinical studies.

Published
2015
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