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7 results on '"Park, Sophie"'

1. Clinical impact of genetic alterations including germline DDX41 mutations in MDS/low-blast count AML patients treated with azacitidine-based regimens

Author

Sébert, Marie, Freiman, Lucie, Chaffaut, Cendrine, Guerci, Agnès, Peterlin, Pierre, Thépot, Sylvain, Beyne-Rauzy, Odile, Park, Sophie, Cluzeau, Thomas, Chermat, Fatiha, Fenaux, Pierre, Preudhomme, Claude, Clappier, Emmanuelle, Chevret, Sylvie, Adès, Lionel, Duployez, Nicolas, and Duchmann, Matthieu

Published
2024
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3. Prospective validation of a biomarker-driven response prediction model to romiplostim in lower-risk myelodysplastic neoplasms – results of the EUROPE trial by EMSCO

Author

Kubasch, Anne Sophie, Giagounidis, Aristoteles, Metzgeroth, Georgia, Jonasova, Anna, Herbst, Regina, Diaz, Jose Miguel Torregrosa, De Renzis, Benoit, Götze, Katharina S., Huetter-Kroenke, Marie-Luise, Gourin, Marie-Pierre, Slama, Borhane, Dimicoli-Salazar, Sophie, Cony-Makhoul, Pascale, Laribi, Kamel, Park, Sophie, Jersemann, Katja, Schipp, Dorothea, Metzeler, Klaus H., Tiebel, Oliver, Sockel, Katja, Gloaguen, Silke, Mies, Anna, Chermat, Fatiha, Thiede, Christian, Sapena, Rosa, Schlenk, Richard F., Fenaux, Pierre, Platzbecker, Uwe, and Adès, Lionel

Published
2022
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4. Extracellular vesicles from myelodysplastic mesenchymal stromal cells induce DNA damage and mutagenesis of hematopoietic stem cells through miRNA transfer

Author

Meunier, Mathieu, Guttin, Audrey, Ancelet, Sarah, Laurin, David, Zannoni, Johanna, Lefebvre, Christine, Tondeur, Sylvie, Persoons, Virginie, Pezet, Mylène, Pernet-Gallay, Karin, Chuffart, Florent, Rousseaux, Sophie, Testard, Quentin, Thevenon, Julien, Jouzier, Claire, Deleuze, Jean-François, Laulagnier, Karine, Sadoul, Rémy, Chatellard, Christine, Hainaut, Pierre, Polack, Benoît, Cahn, Jean-Yves, Issartel, Jean-Paul, and Park, Sophie

Published
2020
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5. Clinical impact of genetic alterations including germline DDX41mutations in MDS/low-blast count AML patients treated with azacitidine-based regimens

Author

Sébert, Marie, Freiman, Lucie, Chaffaut, Cendrine, Guerci, Agnès, Peterlin, Pierre, Thépot, Sylvain, Beyne-Rauzy, Odile, Park, Sophie, Cluzeau, Thomas, Chermat, Fatiha, Fenaux, Pierre, Preudhomme, Claude, Clappier, Emmanuelle, Chevret, Sylvie, Adès, Lionel, Duployez, Nicolas, and Duchmann, Matthieu

Published
2024
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7. Heterogeneous sensitivity of human acute myeloid leukemia to β-catenin down-modulation.

Author

Gandillet A, Park S, Lassailly F, Griessinger E, Vargaftig J, Filby A, Lister TA, and Bonnet D

Subjects
Adult, Aged, Animals, Apoptosis, Blotting, Western, Cell Cycle, Cell Differentiation, Cell Proliferation, Down-Regulation, Female, Flow Cytometry, Humans, Leukemia, Myeloid, Acute genetics, Male, Mice, Mice, Inbred NOD, Mice, SCID, Middle Aged, RNA, Messenger genetics, RNA, Small Interfering genetics, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Transplantation, Heterologous, Tumor Cells, Cultured, beta Catenin antagonists & inhibitors, beta Catenin genetics, Leukemia, Myeloid, Acute metabolism, Leukemia, Myeloid, Acute pathology, beta Catenin metabolism
Abstract

Dysregulation of the Wnt/β-catenin pathway has been observed in various malignancies, including acute myeloid leukemia (AML), where the overexpression of β-catenin is an independent adverse prognostic factor. β-catenin was found upregulated in the vast majority of AML samples and more frequently localized in the nucleus of leukemic stem cells compared with normal bone marrow CD34(+) cells. The knockdown of β-catenin, using a short hairpin RNA (shRNA) lentiviral approach, accelerates all-trans retinoic acid-induced differentiation and impairs the proliferation of HL60 leukemic cell line. Using in vivo quantitative tracking of these cells, we observed a reduced engraftment potential after xenotransplantation when β-catenin was silenced. However, when studying primary AML cells, despite effective downregulation of β-catenin we did not observe any impairment of their in vitro long-term maintenance on MS-5 stroma nor of their engraftment potential in vivo. Altogether, these results show that despite a frequent β-catenin upregulation in AML, leukemia-initiating cells might not be 'addicted' to this pathway and thus targeted therapy against β-catenin might not be successful in all patients.

Published
2011
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