Developmental interplay between transcriptional alterations and a targetable cytokine signaling dependency in pediatric ETO2::GLIS2 leukemia.


Journal

Molecular cancer
ISSN: 1476-4598
Titre abrégé: Mol Cancer
Pays: England
ID NLM: 101147698

Informations de publication

Date de publication:
20 Sep 2024
Historique:
received: 11 06 2024
accepted: 02 09 2024
medline: 21 9 2024
pubmed: 21 9 2024
entrez: 20 9 2024
Statut: epublish

Résumé

Several fusion oncogenes showing a higher incidence in pediatric acute myeloid leukemia (AML) are associated with heterogeneous megakaryoblastic and other myeloid features. Here we addressed how developmental mechanisms influence human leukemogenesis by ETO2::GLIS2, associated with dismal prognosis. We created novel ETO2::GLIS2 models of leukemogenesis through lentiviral transduction and CRISPR-Cas9 gene editing of human fetal and post-natal hematopoietic stem/progenitor cells (HSPCs), performed in-depth characterization of ETO2::GLIS2 transformed cells through multiple omics and compared them to patient samples. This led to a preclinical assay using patient-derived-xenograft models to test a combination of two clinically-relevant molecules. We showed that ETO2::GLIS2 expression in primary human fetal CD34 Our study uncovers an interplay between the cytokine milieu and transcriptional programs that extends a developmental window of permissiveness to transformation by the ETO2::GLIS2 AML fusion oncogene, controls the intratumoral cellular heterogeneity, and offers a ground-breaking therapeutical opportunity by a targeted combination strategy.

Sections du résumé

BACKGROUND BACKGROUND
Several fusion oncogenes showing a higher incidence in pediatric acute myeloid leukemia (AML) are associated with heterogeneous megakaryoblastic and other myeloid features. Here we addressed how developmental mechanisms influence human leukemogenesis by ETO2::GLIS2, associated with dismal prognosis.
METHODS METHODS
We created novel ETO2::GLIS2 models of leukemogenesis through lentiviral transduction and CRISPR-Cas9 gene editing of human fetal and post-natal hematopoietic stem/progenitor cells (HSPCs), performed in-depth characterization of ETO2::GLIS2 transformed cells through multiple omics and compared them to patient samples. This led to a preclinical assay using patient-derived-xenograft models to test a combination of two clinically-relevant molecules.
RESULTS RESULTS
We showed that ETO2::GLIS2 expression in primary human fetal CD34
CONCLUSIONS CONCLUSIONS
Our study uncovers an interplay between the cytokine milieu and transcriptional programs that extends a developmental window of permissiveness to transformation by the ETO2::GLIS2 AML fusion oncogene, controls the intratumoral cellular heterogeneity, and offers a ground-breaking therapeutical opportunity by a targeted combination strategy.

Identifiants

pubmed: 39304903
doi: 10.1186/s12943-024-02110-y
pii: 10.1186/s12943-024-02110-y
doi:

Substances chimiques

Cytokines 0
Oncogene Proteins, Fusion 0
DNA-Binding Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

204

Informations de copyright

© 2024. The Author(s).

Références

de Rooij JDE, Zwaan CM, van den Heuvel-Eibrink M. Pediatric AML: From Biology to Clinical Management. J Clin Med. 2015;4:127–49.
pubmed: 26237023 pmcid: 4470244 doi: 10.3390/jcm4010127
Greaves M. A causal mechanism for childhood acute lymphoblastic leukaemia. Nat Rev Cancer. 2018;18:471–84.
pubmed: 29784935 pmcid: 6986894 doi: 10.1038/s41568-018-0015-6
Wiemels JL, Xiao Z, Buffler PA, Maia AT, Ma X, Dicks BM, et al. In utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemia. Blood. 2002;99:3801–5.
pubmed: 11986239 doi: 10.1182/blood.V99.10.3801
McHale CM, Wiemels JL, Zhang L, Ma X, Buffler PA, Feusner J, et al. Prenatal origin of childhood acute myeloid leukemias harboring chromosomal rearrangements t(15;17) and inv(16). Blood. 2003;101:4640–1.
pubmed: 12756163 doi: 10.1182/blood-2003-01-0313
Schlosser M-P, Bucking S, Lemyre B, Grynspan D, Padmore R, Johnston D. Prenatally Diagnosed Infant AML. J Pediatr Hematol Oncol. 2018;40:238.
pubmed: 28678091 doi: 10.1097/MPH.0000000000000893
Marcotte EL, Spector LG, Mendes-de-Almeida DP, Nelson HH. The Prenatal Origin of Childhood Leukemia: Potential Applications for Epidemiology and Newborn Screening. Front Pediatr. 2021;9:639479. Available from:  https://www.frontiersin.org/articles/10.3389/fped.2021.639479 . Cited 2024 Apr 10.
pubmed: 33968846 pmcid: 8102903 doi: 10.3389/fped.2021.639479
Welch JS, Ley TJ, Link DC, Miller CA, Larson DE, Koboldt DC, et al. The Origin and Evolution of Mutations in Acute Myeloid Leukemia. Cell. 2012;150:264–78.
pubmed: 22817890 pmcid: 3407563 doi: 10.1016/j.cell.2012.06.023
Bolouri H, Farrar JE, Triche T Jr, Ries RE, Lim EL, Alonzo TA, et al. The molecular landscape of pediatric acute myeloid leukemia reveals recurrent structural alterations and age-specific mutational interactions. Nat Med. 2018;24:103–12.
pubmed: 29227476 doi: 10.1038/nm.4439
Notta F, Zandi S, Takayama N, Dobson S, Gan OI, Wilson G, et al. Distinct routes of lineage development reshape the human blood hierarchy across ontogeny. Science. 2016;351:aab2116.
pubmed: 26541609 doi: 10.1126/science.aab2116
Roy A, Wang G, Iskander D, O’Byrne S, Elliott N, O’Sullivan J, et al. Transitions in lineage specification and gene regulatory networks in hematopoietic stem/progenitor cells over human development. Cell Rep. 2021;36:109698.
pubmed: 34525349 pmcid: 8456780 doi: 10.1016/j.celrep.2021.109698
Sommarin MNE, Olofzon R, Palo S, Dhapola P, Soneji S, Karlsson G, et al. Single-cell multiomics of human fetal hematopoiesis defines a developmental specific population and a fetal signature. Blood Advances. 2023;7(18):5325–40.
pubmed: 37379274 pmcid: 10506049 doi: 10.1182/bloodadvances.2023009808
Pagano L, Pulsoni A, Vignetti M, Mele L, Fianchi L, Petti MC, et al. Acute megakaryoblastic leukemia: experience of GIMEMA trials. Leukemia. 2002;16:1622–6.
pubmed: 12200673 doi: 10.1038/sj.leu.2402618
McNulty M, Crispino JD. Acute Megakaryocytic Leukemia. Cold Spring Harb Perspect Med. 2020;10:a034884.
pubmed: 31548219 pmcid: 6996441 doi: 10.1101/cshperspect.a034884
de Rooij JDE, Branstetter C, Ma J, Li Y, Walsh MP, Cheng J, et al. Pediatric non–Down syndrome acute megakaryoblastic leukemia is characterized by distinct genomic subsets with varying outcomes. Nat Genet. 2017;49:451–6.
pubmed: 28112737 pmcid: 5687824 doi: 10.1038/ng.3772
Lopez CK, Noguera E, Stavropoulou V, Robert E, Aid Z, Ballerini P, et al. Ontogenic Changes in Hematopoietic Hierarchy Determine Pediatric Specificity and Disease Phenotype in Fusion Oncogene-Driven Myeloid Leukemia. Cancer Discov. 2019;9:1736–53.
pubmed: 31662298 doi: 10.1158/2159-8290.CD-18-1463
Gruber TA, Larson Gedman A, Zhang J, Koss CS, Marada S, Ta HQ, et al. An Inv(16)(p13.3q24.3)-Encoded CBFA2T3-GLIS2 Fusion Protein Defines an Aggressive Subtype of Pediatric Acute Megakaryoblastic Leukemia. Cancer Cell. 2012;22:683–97.
pubmed: 23153540 pmcid: 3547667 doi: 10.1016/j.ccr.2012.10.007
Thiollier C, Lopez CK, Gerby B, Ignacimouttou C, Poglio S, Duffourd Y, et al. Characterization of novel genomic alterations and therapeutic approaches using acute megakaryoblastic leukemia xenograft models. J Exp Med. 2012;209:2017–31.
pubmed: 23045605 pmcid: 3478932 doi: 10.1084/jem.20121343
Thirant C, Ignacimouttou C, Lopez CK, Diop M, Le Mouël L, Thiollier C, et al. ETO2-GLIS2 Hijacks Transcriptional Complexes to Drive Cellular Identity and Self-Renewal in Pediatric Acute Megakaryoblastic Leukemia. Cancer Cell. 2017;31:452–65.
pubmed: 28292442 doi: 10.1016/j.ccell.2017.02.006
Thirant C, Lopez C, Malinge S, Mercher T. Molecular pathways driven by ETO2-GLIS2 in aggressive pediatric leukemia. Molecular & Cellular Oncology. 2017;4:e1345351.
doi: 10.1080/23723556.2017.1345351
Benbarche S, Lopez CK, Salataj E, Aid Z, Thirant C, Laiguillon M-C, et al. Screening of ETO2-GLIS2–induced Super Enhancers identifies targetable cooperative dependencies in acute megakaryoblastic leukemia. Science Adv. 2022;8:eabg9455.
doi: 10.1126/sciadv.abg9455
Aid Z, Robert E, Lopez CK, Bourgoin M, Boudia F, Le Mene M, et al. High caspase 3 and vulnerability to dual BCL2 family inhibition define ETO2::GLIS2 pediatric leukemia. Leukemia. 2023;37:571–9.
pubmed: 36585521 doi: 10.1038/s41375-022-01800-0
Gress V, Roussy M, Boulianne L, Bilodeau M, Cardin S, EL-Hachem N, et al. CBFA2T3::GLIS2 Pediatric Acute Megakaryoblastic Leukemia is Sensitive to BCL-XL Inhibition by Navitoclax and DT2216. Blood Adv. 2023;8(1):112–29.
pmcid: 10787250 doi: 10.1182/bloodadvances.2022008899
Neault M, Lebert-Ghali C-É, Fournier M, Capdevielle C, Garfinkle EAR, Obermayer A, et al. CBFA2T3-GLIS2-dependent pediatric acute megakaryoblastic leukemia is driven by GLIS2 and sensitive to navitoclax. Cell Rep. 2023;42:113084.
pubmed: 37716355 doi: 10.1016/j.celrep.2023.113084
Masetti R, Pigazzi M, Togni M, Astolfi A, Indio V, Manara E, et al. CBFA2T3-GLIS2 fusion transcript is a novel common feature in pediatric, cytogenetically normal AML, not restricted to FAB M7 subtype. Blood. 2013;121:3469–72.
pubmed: 23407549 doi: 10.1182/blood-2012-11-469825
Noort S, Wander P, Alonzo TA, Smith J, Ries RE, Gerbing RB, et al. The clinical and biological characteristics of NUP98-KDM5A in pediatric acute myeloid leukemia. Haematologica. 2021;106:630–4.
pubmed: 32381579 doi: 10.3324/haematol.2019.236745
Smith JL, Ries RE, Hylkema T, Alonzo TA, Gerbing RB, Santaguida MT, et al. Comprehensive Transcriptome Profiling of Cryptic CBFA2T3–GLIS2 Fusion-Positive AML Defines Novel Therapeutic Options: A COG and TARGET Pediatric AML Study. Clin Cancer Res. 2020;26:726–37.
pubmed: 31719049 doi: 10.1158/1078-0432.CCR-19-1800
Wagenblast E, Araújo J, Gan OI, Cutting SK, Murison A, Krivdova G, et al. Mapping the cellular origin and early evolution of leukemia in Down syndrome. Science. 2021;373:eabf6202.
pubmed: 34244384 doi: 10.1126/science.abf6202
Sirven A, Ravet E, Charneau P, Zennou V, Coulombel L, Guétard D, et al. Enhanced Transgene Expression in Cord Blood CD34+-Derived Hematopoietic Cells, Including Developing T Cells and NOD/SCID Mouse Repopulating Cells, Following Transduction with Modified TRIP Lentiviral Vectors. Mol Ther. 2001;3:438–48.
pubmed: 11319904 doi: 10.1006/mthe.2001.0282
Gerby B, Armstrong F, de la Grange PB, Medyouf H, Calvo J, Verhoeyen E, et al. Optimized gene transfer into human primary leukemic T cell with NOD-SCID/leukemia-initiating cell activity. Leukemia. 2010;24:646–9.
pubmed: 19924146 doi: 10.1038/leu.2009.235
Babin L, Darchen A, Robert E, Aid Z, Borry R, Soudais C, et al. De novo generation of the NPM-ALK fusion recapitulates the pleiotropic phenotypes of ALK+ ALCL pathogenesis and reveals the ROR2 receptor as target for tumor cells. Mol Cancer. 2022;21:65.
pubmed: 35246138 pmcid: 8895835 doi: 10.1186/s12943-022-01520-0
Renouf B, Piganeau M, Ghezraoui H, Jasin M, Brunet E. Creating cancer translocations in human cells using Cas9 DSBs and nCas9 paired nicks. Methods Enzymol. 2014;546:251–71.
pubmed: 25398344 pmcid: 4398311 doi: 10.1016/B978-0-12-801185-0.00012-X
McIntosh BE, Brown ME, Duffin BM, Maufort JP, Vereide DT, Slukvin II, et al. Nonirradiated NOD,B6.SCID Il2rγ−/−KitW41/W41 (NBSGW) mice support multilineage engraftment of human hematopoietic cells. Stem Cell Rep. 2015;4:171–80.
doi: 10.1016/j.stemcr.2014.12.005
Buenrostro JD, Giresi PG, Zaba LC, Chang HY, Greenleaf WJ. Transposition of native chromatin for fast and sensitive epigenomic profiling of open chromatin, DNA-binding proteins and nucleosome position. Nat Methods. 2013;10:1213–8.
pubmed: 24097267 pmcid: 3959825 doi: 10.1038/nmeth.2688
Parkhomchuk D, Borodina T, Amstislavskiy V, Banaru M, Hallen L, Krobitsch S, et al. Transcriptome analysis by strand-specific sequencing of complementary DNA. Nucleic Acids Res. 2009;37:e123.
pubmed: 19620212 pmcid: 2764448 doi: 10.1093/nar/gkp596
Hafemeister C, Satija R. Normalization and variance stabilization of single-cell RNA-seq data using regularized negative binomial regression. Genome Biol. 2019;20:296.
pubmed: 31870423 pmcid: 6927181 doi: 10.1186/s13059-019-1874-1
Arkoun B, Robert E, Boudia F, Mazzi S, Dufour V, Siret A, et al. Stepwise GATA1 and SMC3 mutations alter megakaryocyte differentiation in a Down syndrome leukemia model. J Clin Invest. 2022;132(14):e156290.
pubmed: 35587378 pmcid: 9282925 doi: 10.1172/JCI156290
Bourquin J-P, Subramanian A, Langebrake C, Reinhardt D, Bernard O, Ballerini P, et al. Identification of distinct molecular phenotypes in acute megakaryoblastic leukemia by gene expression profiling. Proc Natl Acad Sci USA. 2006;103:3339.
pubmed: 16492768 pmcid: 1413912 doi: 10.1073/pnas.0511150103
Paredes-Aguilera R, Romero-Guzman L, Lopez-Santiago N, Trejo RA. Biology, clinical, and hematologic features of acute megakaryoblastic leukemia in children. Am J Hematol. 2003;73:71–80.
pubmed: 12749007 doi: 10.1002/ajh.10320
Ishibashi M, Yokosuka T, Yanagimachi MD, Iwasaki F, Tsujimoto S, Sasaki K, et al. Clinical Courses of Two Pediatric Patients with Acute Megakaryoblastic Leukemia Harboring the CBFA2T3-GLIS2 Fusion Gene. Turk J Haematol. 2016;33:331–4.
pubmed: 27094503 pmcid: 5204189 doi: 10.4274/tjh.2016.0008
Hara Y, Shiba N, Ohki K, Tabuchi K, Yamato G, Park M, et al. Prognostic impact of specific molecular profiles in pediatric acute megakaryoblastic leukemia in non-Down syndrome. Genes Chromosom Cancer. 2017;56:394–404.
pubmed: 28063190 doi: 10.1002/gcc.22444
Wunderlich M, Chou F-S, Sexton C, Presicce P, Chougnet CA, Aliberti J, et al. Improved multilineage human hematopoietic reconstitution and function in NSGS mice. PLoS ONE. 2018;13: e0209034.
pubmed: 30540841 pmcid: 6291127 doi: 10.1371/journal.pone.0209034
Martinez-Soria N, McKenzie L, Draper J, Ptasinska A, Issa H, Potluri S, et al. The Oncogenic Transcription Factor RUNX1/ETO Corrupts Cell Cycle Regulation to Drive Leukemic Transformation. Cancer Cell. 2018;34:626-642.e8.
pubmed: 30300583 pmcid: 6179967 doi: 10.1016/j.ccell.2018.08.015
Hara T, Miyajima A. Function and Signal Transduction Mediated by the Interleukin 3 Receptor System in Hematopoiesis. Stem Cells. 1996;14:605–18.
pubmed: 8948019 doi: 10.1002/stem.140605
Wilkes MC, Shibuya A, Sakamoto KM. Signaling Pathways That Regulate Normal and Aberrant Red Blood Cell Development. Genes (Basel). 2021;12:1646.
pubmed: 34681039 doi: 10.3390/genes12101646
Liang J, Wu Y-L, Chen B-J, Zhang W, Tanaka Y, Sugiyama H. The C-Kit Receptor-Mediated Signal Transduction and Tumor-Related Diseases. Int J Biol Sci. 2013;9:435–43.
pubmed: 23678293 pmcid: 3654492 doi: 10.7150/ijbs.6087
Yoshida T, Kakegawa J, Yamaguchi T, Hantani Y, Okajima N, Sakai T, et al. Identification and Characterization of a Novel Chemotype MEK Inhibitor Able to Alter the Phosphorylation State of MEK1/2. Oncotarget. 2012;3:1533–45.
pubmed: 23237773 pmcid: 3681492 doi: 10.18632/oncotarget.747
Le Q, Hadland B, Smith JL, Leonti A, Huang BJ, Ries R, et al. CBFA2T3-GLIS2 model of pediatric acute megakaryoblastic leukemia identifies FOLR1 as a CAR T cell target. J Clin Invest. 2022;132(22):e157101. Available from:  https://www.jci.org/articles/view/157101 . Cited 2024 Feb 21.
pubmed: 36136600 pmcid: 9663156 doi: 10.1172/JCI157101
Rice S, Jackson T, Crump NT, Fordham N, Elliott N, O’Byrne S, et al. A human fetal liver-derived infant MLL-AF4 acute lymphoblastic leukemia model reveals a distinct fetal gene expression program. Nat Commun. 2021;12:6905.
pubmed: 34824279 pmcid: 8616957 doi: 10.1038/s41467-021-27270-z
Bueno C, Torres-Ruíz R, Velasco-Hernandez T, Molina O, Petazzi P, Martinez-Moreno A, et al. A human genome editing-based MLL::AF4 B-cell ALL model recapitulates key cellular and molecular leukemogenic features. Blood. 2023;142(20):1752–6.
pubmed: 37756522 doi: 10.1182/blood.2023020858
Secker K-A, Bruns L, Keppeler H, Jeong J, Hentrich T, Schulze-Hentrich JM, et al. Only Hematopoietic Stem and Progenitor Cells from Cord Blood Are Susceptible to Malignant Transformation by MLL-AF4 Translocations. Cancers. 2020;12:1487.
pubmed: 32517300 pmcid: 7352867 doi: 10.3390/cancers12061487
Li Z, Godinho FJ, Klusmann J-H, Garriga-Canut M, Yu C, Orkin SH. Developmental stage–selective effect of somatically mutated leukemogenic transcription factor GATA1. Nat Genet. 2005;37:613–9.
pubmed: 15895080 doi: 10.1038/ng1566
Zhou BO, Yu H, Yue R, Zhao Z, Rios JJ, Naveiras O, et al. Bone marrow adipocytes promote the regeneration of stem cells and haematopoiesis by secreting SCF. Nat Cell Biol. 2017;19:891–903.
pubmed: 28714970 pmcid: 5536858 doi: 10.1038/ncb3570
Xu C, Gao X, Wei Q, Nakahara F, Zimmerman SE, Mar J, et al. Stem cell factor is selectively secreted by arterial endothelial cells in bone marrow. Nat Commun. 2018;9:2449.
pubmed: 29934585 pmcid: 6015052 doi: 10.1038/s41467-018-04726-3
Lee Y, Leslie J, Yang Y, Ding L. Hepatic stellate and endothelial cells maintain hematopoietic stem cells in the developing liver. J Exp Med. 2021;218:e20200882.
pubmed: 33151261 doi: 10.1084/jem.20200882
Varricchi G, Poto R, Marone G, Schroeder JT. IL-3 in the development and function of basophils. Semin Immunol. 2021;54:101510.
pubmed: 34756806 doi: 10.1016/j.smim.2021.101510
Kiss MG, Mindur JE, Yates AG, Lee D, Fullard JF, Anzai A, et al. Interleukin-3 coordinates glial-peripheral immune crosstalk to incite multiple sclerosis. Immunity. 2023;56:1502-1514.e8.
pubmed: 37160117 pmcid: 10524830 doi: 10.1016/j.immuni.2023.04.013
Wunderlich M, Chou F-S, Link KA, Mizukawa B, Perry RL, Carroll M, et al. AML xenograft efficiency is significantly improved in NOD/SCID-IL2RG mice constitutively expressing human SCF, GM-CSF and IL-3. Leukemia. 2010;24:1785–8.
pubmed: 20686503 pmcid: 5439963 doi: 10.1038/leu.2010.158
Sadras T, Perugini M, Kok CH, Iarossi DG, Heatley SL, Brumatti G, et al. Interleukin-3-mediated regulation of β-catenin in myeloid transformation and acute myeloid leukemia. J Leukoc Biol. 2014;96:83–91.
pubmed: 24598054 doi: 10.1189/jlb.2AB1013-559R
Bulaeva E, Pellacani D, Nakamichi N, Hammond CA, Beer PA, Lorzadeh A, et al. MYC-induced human acute myeloid leukemia requires a continuing IL-3/GM-CSF costimulus. Blood. 2020;136:2764–73.
pubmed: 33301029 doi: 10.1182/blood.2020006374
Fan AC, Nakauchi Y, Bai L, Azizi A, Nuno KA, Zhao F, et al. RUNX1 loss renders hematopoietic and leukemic cells dependent on IL-3 and sensitive to JAK inhibition. J Clin Invest. 2023;133:e167053.
pubmed: 37581927 pmcid: 10541186 doi: 10.1172/JCI167053
Carey A, Edwards DK, Eide CA, Newell L, Traer E, Medeiros BC, et al. Identification of Interleukin-1 by Functional Screening as a Key Mediator of Cellular Expansion and Disease Progression in Acute Myeloid Leukemia. Cell Rep. 2017;18:3204–18.
pubmed: 28355571 pmcid: 5437102 doi: 10.1016/j.celrep.2017.03.018
Meisel M, Hinterleitner R, Pacis A, Chen L, Earley ZM, Mayassi T, et al. Microbial signals drive pre-leukaemic myeloproliferation in a Tet2-deficient host. Nature. 2018;557:580–4.
pubmed: 29769727 pmcid: 6238954 doi: 10.1038/s41586-018-0125-z
Hay SB, Ferchen K, Chetal K, Grimes HL, Salomonis N. The Human Cell Atlas bone marrow single-cell interactive web portal. Exp Hematol. 2018;68:51–61.
pubmed: 30243574 pmcid: 6296228 doi: 10.1016/j.exphem.2018.09.004

Auteurs

Verónica Alonso-Pérez (V)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Laboratoire Des Cellules Souches Hématopoïétiques Et Des Leucémies, Équipe Labellisée Ligue Contre Le Cancer, Equipe Niche Et Cancer Dans L'Hématopoïèse, Unité Mixte de Recherche (UMR) 1274 INSERM, CEA, 18 route du panorama, Fontenay-Aux Roses, F-92265, France.

Klaudia Galant (K)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Laboratoire Des Cellules Souches Hématopoïétiques Et Des Leucémies, Équipe Labellisée Ligue Contre Le Cancer, Equipe Niche Et Cancer Dans L'Hématopoïèse, Unité Mixte de Recherche (UMR) 1274 INSERM, CEA, 18 route du panorama, Fontenay-Aux Roses, F-92265, France.

Fabien Boudia (F)

INSERM U1170, Gustave Roussy, Université Paris-Saclay, PEDIAC Program, Equipe Labellisée Ligue Contre Le Cancer, Villejuif, France.

Elie Robert (E)

INSERM U1170, Gustave Roussy, Université Paris-Saclay, PEDIAC Program, Equipe Labellisée Ligue Contre Le Cancer, Villejuif, France.

Zakia Aid (Z)

INSERM U1170, Gustave Roussy, Université Paris-Saclay, PEDIAC Program, Equipe Labellisée Ligue Contre Le Cancer, Villejuif, France.

Laurent Renou (L)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Laboratoire Des Cellules Souches Hématopoïétiques Et Des Leucémies, Équipe Labellisée Ligue Contre Le Cancer, Equipe Niche Et Cancer Dans L'Hématopoïèse, Unité Mixte de Recherche (UMR) 1274 INSERM, CEA, 18 route du panorama, Fontenay-Aux Roses, F-92265, France.

Vilma Barroca (V)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Animal Experimentation Platform, IRCM, CEA, Fontenay-Aux-Roses, F-92260, France.

Saryiami Devanand (S)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Animal Experimentation Platform, IRCM, CEA, Fontenay-Aux-Roses, F-92260, France.

Loélia Babin (L)

Laboratory of theGenome Dynamics in the Immune System, Équipe Labellisée Ligue Contre Le Cancer, Université Paris Cité, Université Paris-Saclay, INSERM UMR 1163, Institut Imagine, Paris, France.

Virginie Rouiller-Fabre (V)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.

Delphine Moison (D)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.

Didier Busso (D)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Cigex Molecular Platform, IRCM, CEA, IBFJ, Fontenay-Aux-Roses, France.

Guillaume Piton (G)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Cigex Molecular Platform, IRCM, CEA, IBFJ, Fontenay-Aux-Roses, France.

Christophe Metereau (C)

INSERM U1170, Gustave Roussy, Université Paris-Saclay, PEDIAC Program, Equipe Labellisée Ligue Contre Le Cancer, Villejuif, France.

Nassera Abermil (N)

Centre de Recherche Saint-Antoine, CRSA, SIRIC CURAMUS, Hôpital Saint-Antoine, Service d'Hématologie Biologique, Sorbonne Université, 75012, Paris, France.

Paola Ballerini (P)

Department of Pediatric Hematology-Oncology, Hôpital Armand Trousseau, AP-HP, Paris, France.

Pierre Hirsch (P)

Centre de Recherche Saint-Antoine, CRSA, SIRIC CURAMUS, Hôpital Saint-Antoine, Service d'Hématologie Biologique, Sorbonne Université, 75012, Paris, France.

Rima Haddad (R)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France.
Laboratoire Des Cellules Souches Hématopoïétiques Et Des Leucémies, Équipe Labellisée Ligue Contre Le Cancer, Equipe Niche Et Cancer Dans L'Hématopoïèse, Unité Mixte de Recherche (UMR) 1274 INSERM, CEA, 18 route du panorama, Fontenay-Aux Roses, F-92265, France.

Jelena Martinovic (J)

Unit of Fetal Pathology, Hôpital Antoine Beclère, AP-HP, Clamart, France.

Arnaud Petit (A)

Department of Pediatric Hematology-Oncology, Hôpital Armand Trousseau, AP-HP, Paris, France.

Hélène Lapillonne (H)

Department of Pediatric Hematology-Oncology, Hôpital Armand Trousseau, AP-HP, Paris, France.

Erika Brunet (E)

Laboratory of theGenome Dynamics in the Immune System, Équipe Labellisée Ligue Contre Le Cancer, Université Paris Cité, Université Paris-Saclay, INSERM UMR 1163, Institut Imagine, Paris, France.

Thomas Mercher (T)

INSERM U1170, Gustave Roussy, Université Paris-Saclay, PEDIAC Program, Equipe Labellisée Ligue Contre Le Cancer, Villejuif, France. thomas.mercher@gustaveroussy.fr.
OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France. thomas.mercher@gustaveroussy.fr.

Françoise Pflumio (F)

Commissariat À L'Energie Atomique Et Aux Energies Alternatives (CEA), Université Paris Cité, Institut National de La Santé Et de La Recherche Médicale (INSERM), Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France. francoise.pflumio@cea.fr.
Université Paris-Saclay, INSERM, CEA, Stabilité Génétique Cellules Souches Et Radiations, Fontenay-Aux-Roses, F-92260, France. francoise.pflumio@cea.fr.
Laboratoire Des Cellules Souches Hématopoïétiques Et Des Leucémies, Équipe Labellisée Ligue Contre Le Cancer, Equipe Niche Et Cancer Dans L'Hématopoïèse, Unité Mixte de Recherche (UMR) 1274 INSERM, CEA, 18 route du panorama, Fontenay-Aux Roses, F-92265, France. francoise.pflumio@cea.fr.
OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France. francoise.pflumio@cea.fr.

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