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1. Data from BCL-2 and Mutant NRAS Interact Physically and Functionally in a Mouse Model of Progressive Myelodysplasia

Author

Omidvar, Nader, primary, Kogan, Scott, primary, Beurlet, Stephanie, primary, le Pogam, Carole, primary, Janin, Anne, primary, West, Robert, primary, Noguera, Maria-Elena, primary, Reboul, Murielle, primary, Soulie, Annie, primary, Leboeuf, Christophe, primary, Setterblad, Niclas, primary, Felsher, Dean, primary, Lagasse, Eric, primary, Mohamedali, Azim, primary, Thomas, N. Shaun B., primary, Fenaux, Pierre, primary, Fontenay, Michaela, primary, Pla, Marika, primary, Mufti, Ghulam J., primary, Weissman, Irving, primary, Chomienne, Christine, primary, and Padua, Rose Ann, primary

Published
2023
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2. Supplementary Procedures, Figures 1-4 from BCL-2 and Mutant NRAS Interact Physically and Functionally in a Mouse Model of Progressive Myelodysplasia

Author

Omidvar, Nader, primary, Kogan, Scott, primary, Beurlet, Stephanie, primary, le Pogam, Carole, primary, Janin, Anne, primary, West, Robert, primary, Noguera, Maria-Elena, primary, Reboul, Murielle, primary, Soulie, Annie, primary, Leboeuf, Christophe, primary, Setterblad, Niclas, primary, Felsher, Dean, primary, Lagasse, Eric, primary, Mohamedali, Azim, primary, Thomas, N. Shaun B., primary, Fenaux, Pierre, primary, Fontenay, Michaela, primary, Pla, Marika, primary, Mufti, Ghulam J., primary, Weissman, Irving, primary, Chomienne, Christine, primary, and Padua, Rose Ann, primary

Published
2023
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3. BCL-2 inhibition with ABT-737 prolongs survival in an NRAS/BCL-2 mouse model of AML by targeting primitive LSK and progenitor cells

Author

Beurlet, Stephanie, Omidvar, Nader, Gorombei, Petra, Krief, Patricia, Le Pogam, Carole, Setterblad, Niclas, de la Grange, Pierre, Leboeuf, Christophe, Janin, Anne, Noguera, Maria-Elena, Hervatin, Florence, Sarda-Mantel, Laure, Konopleva, Marina, Andreeff, Michael, Tu, Andrea W., Fan, Alice C., Felsher, Dean W., Whetton, Anthony, Pla, Marika, West, Robert, Fenaux, Pierre, Chomienne, Christine, and Padua, Rose Ann

Published
2013
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4. Localization of the NRAS:BCL-2 complex determines anti-apoptotic features associated with progressive disease in myelodysplastic syndromes

Author

Le Pogam, Carole, Krief, Patricia, Beurlet, Stephanie, Soulié, Annie, Balitrand, Nicole, Cassinat, Bruno, Cavé, Helene, Kosmider, Olivier, Setterblad, Niclas, Leboeuf, Christophe, Sarda-Mantel, Laure, Hervatin, Florence, Merlet, Pascal, Noguera, Maria-Elena, Janin, Anne, Pla, Marika, Fontenay, Michaela, Adès, Lionel, Fenaux, Pierre, Chomienne, Christine, Padua, Rose Ann, and Omidvar, Nader

Published
2013
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6. BCL-2 Inhibitor ABT-737 Effectively Targets Leukemia-Initiating Cells with Differential Regulation of Relevant Genes Leading to Extended Survival in a NRAS/BCL-2 Mouse Model of High Risk-Myelodysplastic Syndrome

Author

Gorombei, Petra, primary, Guidez, Fabien, additional, Ganesan, Saravanan, additional, Chiquet, Mathieu, additional, Pellagatti, Andrea, additional, Goursaud, Laure, additional, Tekin, Nilgun, additional, Beurlet, Stephanie, additional, Patel, Satyananda, additional, Guerenne, Laura, additional, Le Pogam, Carole, additional, Setterblad, Niclas, additional, de la Grange, Pierre, additional, LeBoeuf, Christophe, additional, Janin, Anne, additional, Noguera, Maria-Elena, additional, Sarda-Mantel, Laure, additional, Merlet, Pascale, additional, Boultwood, Jacqueline, additional, Konopleva, Marina, additional, Andreeff, Michael, additional, West, Robert, additional, Pla, Marika, additional, Adès, Lionel, additional, Fenaux, Pierre, additional, Krief, Patricia, additional, Chomienne, Christine, additional, Omidvar, Nader, additional, and Padua, Rose Ann, additional

Published
2021
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7. Spontaneous abrogation of the [G.sub.2] DNA damage checkpoint has clinical benefits but promotes leukemogenesis in Fanconi anemia patients

Author

Ceccaldi, Raphael, Briot, Delphine, Larghero, Jerome, Vasquez, Nadia, d'Enghien, Catherine Dubois, Chamousset, Delphine, Noguera, Maria-Elena, Waisfisz, Quinten, Hermine, Olivier, Pondarre, Corinne, Leblanc, Thierry, Gluckman, Eliane, Joenje, Hans, Stoppa-Lyonnet, Dominique, Socie, Gerard, and Soulier, Jean

Subjects
Leukemia -- Risk factors -- Development and progression -- Research -- Genetic aspects, Fanconi's anemia -- Genetic aspects -- Development and progression -- Complications and side effects -- Research, DNA damage -- Research, Health care industry
Abstract

DNA damage checkpoints in the cell cycle may be important barriers against cancer progression in human cells. Fanconi anemia (FA) is an inherited DNA instability disorder that is associated with bone marrow failure and a strong predisposition to cancer. Although FA cells experience constitutive chromosomal breaks, cell cycle arrest at the [G.sub.2] DNA damage checkpoint, and an excess of cell death, some patients do become clinically stable, and the mechanisms underlying this, other than spontaneous reversion of the disease-causing mutation, are not well understood. Here we have defined a clonal phenotype, termed attenuation, in which FA patients acquire an abrogation of the [G.sub.2] checkpoint arrest. Attenuated cells expressed lower levels of CHK1 (also known as CHEK1) and p53. The attenuation could be recapitulated by modulating the ATR/CHK1 pathway, and CHK1 inhibition protected FA cells from cell death. FA patients who expressed the attenuated phenotype had mild bone marrow deficiency and reached adulthood, but several of them eventually developed myelodysplasia or leukemia. Better understanding of attenuation might help predict a patient's clinical course and guide choice of treatment. Our results also highlight the importance of evaluating the cellular DNA damage checkpoint and repair pathways in cancer therapies in general., Introduction Checkpoint pathways are complex biological pathways that regulate responses to DNA damage and other cellular events (1-3). The typical DNA damage checkpoint response triggers cell cycle arrest, allowing time [...]

Published
2011
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10. Splenic marginal zone lymphoma: current knowledge and future directions

Author

Thieblemont, Catherine, Davi, Frederic, Noguera, Maria-Elena, Briere, Josette, Bertoni, Francesco, Zucca, Emanuele, Traverse-Glehen, Alexandra, Felman, Pascale, Berger, Francoise, Salles, Gilles, and Coiffier, Bertrand

Subjects
Non-Hodgkin's lymphomas -- Development and progression -- Diagnosis -- Health aspects, Hepatitis C virus -- Health aspects, Hepatitis C -- Development and progression -- Diagnosis -- Health aspects, Health, World Health Organization
Abstract

Splenic marginal zone lymphoma (SMZL), along with extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) and nodal marginal zone lymphoma (NMZL), share a common origin from the 'marginal zone.' However, these three entities display different clinical characteristics, reflecting probable biological variations according to the organ and cellular origin. Within the past decade, new data have been reported regarding pathogenic mechanisms as well as therapeutic advances. Clinically, SMZL presents as an indolent and disseminated disease at diagnosis, with a specific clinical presentation that includes predominantly splenomegaly, and in half of patients, autoimmune manifestations. Establishing the diagnosis may be difficult, especially distinguishing SMZL from other low-grade lymphomas, such as small B-cell lymphomas; however, recent findings have contributed to a better characterization of the disease, and the criteria for diagnosis have been improved. Therapeutic approaches consist of splenectomy or immunochemotherapy, but there is no consensus regarding the best treatment, except when SMZL is associated with hepatitis C virus infection. In this article, we review the current knowledge on the biological findings, clinical features, and therapeutic approaches for SMZL., Introduction Marginal zone lymphomas (MZLs) represent a group of lymphoid tumors that originate from memory B lymphocytes normally present in a distinct microanatomic compartment, the so-called marginal zone (MZ) of [...]

Published
2012

11. GEP analysis validates high risk MDS and acute myeloid leukemia post MDS mice models and highlights novel dysregulated pathways

Author

Guerenne, Laura, primary, Beurlet, Stéphanie, additional, Said, Mohamed, additional, Gorombei, Petra, additional, Le Pogam, Carole, additional, Guidez, Fabien, additional, de la Grange, Pierre, additional, Omidvar, Nader, additional, Vanneaux, Valérie, additional, Mills, Ken, additional, Mufti, Ghulam J, additional, Sarda-Mantel, Laure, additional, Noguera, Maria Elena, additional, Pla, Marika, additional, Fenaux, Pierre, additional, Padua, Rose Ann, additional, Chomienne, Christine, additional, and Krief, Patricia, additional

Published
2016
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12. Biological Description of 109 Cases of Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN) from the French Network of BPDCN

Author

Poret, Eve, primary, Angelot Delettre, Fanny, additional, Biichle, Sabeha, additional, Roogy, Anne, additional, Benazet, Louis, additional, Pagadoy, Maider, additional, Vidal, Chrystelle, additional, Leroux, Franck, additional, Harrivel, Véronique, additional, Ferrand, Christophe, additional, Salaun, Veronique, additional, Benseddik, Zehaira, additional, Guy, Julien, additional, Jacob, Marie Christine, additional, Roumier, Christophe, additional, Feuillard, Jean, additional, Vila, Liliana, additional, Baseggio, Lucile, additional, Plesa, Adriana, additional, Arnoulet, Christine, additional, Benet, B, additional, Drenou, Bernard, additional, Latger Cannard, Veronique, additional, Bene, Marie-Christine, additional, Ticchioni, Michel, additional, Lusina, Daniel, additional, Bardet, Valerie, additional, LE Garff Tavernier, Magalie, additional, Macintyre, Elizabeth, additional, Asnafi, Vahid, additional, Noguera, Maria Elena, additional, Bouyer, Sabrina, additional, Lecoq Lafon, Carine, additional, Roussel, Mikael, additional, Jardin, Fabrice, additional, Solly, Francoise, additional, Campos, Lydia, additional, Galoisy, Anne, additional, Arnaud, Anne, additional, Daliphard, Sylvie, additional, Genevieve, Franck, additional, Lacroix, Romaric, additional, Schillinger, Françoise, additional, Seilles, Estelle, additional, Binda, Delphine, additional, Deconinck, Eric, additional, Saas, Philippe, additional, and Garnache Ottou, Francine, additional

Published
2015
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13. Mutual benefits of B-ALL and HLDA/HCDM HLDA 9th Barcelona 2010

Author

Faure, Gilbert C, Amsellem, Sophie, Arnoulet, Christine, Bardet, Valérie, Campos, Lydia, De Carvalho-Bittencourt, Marcelo, De Labarthe, Adrienne, Eischen, Alice, Feuillard, Jean, Fossat, Chantal, Ottou, Francine Garnache, Guérin, Estelle, Guy, Julien, Jouault, Hélène, Kuhlein, Emilienne, Lacombe, Francis, Lainey, Elodie, Maynadié, Marc, Noguera, Maria Elena, Roussel, Mikael, Solly, Françoise, Ballon, Orianne Wagner, Béné, Marie C, Renseigné, Non, Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), and Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Adult, Adolescent, Lymphoblastic Leukemia, Immunology, Immunophenotyping, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Antigen, Antigens, CD, Immunology and Allergy, Medicine, Humans, Child, 030304 developmental biology, Aged, Aged, 80 and over, 0303 health sciences, business.industry, Gene Expression Profiling, Antibodies, Monoclonal, Infant, Middle Aged, Precursor Cell Lymphoblastic Leukemia-Lymphoma, 3. Good health, Gene Expression Regulation, Child, Preschool, [SDV.IMM]Life Sciences [q-bio]/Immunology, business, Clone (B-cell biology), 030215 immunology
Abstract

International audience; The B-cell panel of the ninth HLDA was applied in a multicentre fashion to cryopreserved cells from 46 patients with acute lymphoblastic leukemia. The reagents were aliquoted and shipped to volunteer participants from the French Groupe d'Etude Immunologique des Leucémies (GEIL). All samples were tested in flow cytometry, and the results collected as of the strength of labeling of the leukemic clone as negative, weak or strong. Among the 64 antibodies tested, the strongest and most frequent staining was observed for CD305 (LAIR), CD229 (Ly9), CD200 (OX-2) and, to a lesser extent, CD361 (EVI2b). Details of the observations, and information about the molecules tested are provided in the manuscript as well as a summary table.

Published
2011

14. DNA-mediated adjuvant immunotherapy extends survival in two different mouse models of myeloid malignancies

Author

Le Pogam, Carole, primary, Patel, Satyananda, additional, Gorombei, Petra, additional, Guerenne, Laura, additional, Krief, Patricia, additional, Omidvar, Nader, additional, Tekin, Nilgun, additional, Bernasconi, Elena, additional, Sicre, Flore, additional, Schlageter, Marie-Helene, additional, Chopin, Martine, additional, Noguera, Maria-Elena, additional, West, Robert, additional, Abu, Ansu, additional, Mathews, Vikram, additional, Pla, Marika, additional, Fenaux, Pierre, additional, Chomienne, Christine, additional, and Padua, Rose Ann, additional

Published
2015
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15. Efficacy of ABT-737, a BCL-2 Inhibitor, in an NRAS/BCL2 Mouse Model of High Risk Myelodysplasia (HR-MDS) By Targeting Pathways Identified By Gene Expression Profiling

Author

Padua, Rose Ann, primary, Gorombei, Petra, additional, Beurlet, Stéphanie, additional, Omidvar, Nader, additional, Patel, Satyananda, additional, Guerenne, Laura, additional, Le Pogam, Carole, additional, Setterblad, Niclas, additional, de la Grange, Pierre, additional, Guidez, Fabien, additional, Le Boeuf, Christophe, additional, Janin, Anne, additional, Noguera, Maria-Elena, additional, Sarda-Mantel, Laure, additional, Merlet, Pascal, additional, West, Robert, additional, Pla, Marika, additional, Fenaux, Pierre, additional, Krief, Patricia, additional, and Chomienne, Christine, additional

Published
2014
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16. Un cas de myélome phagocytaire et revue de la littérature.

Author

Brumpt, Caren, Baron, Marine, Vignon, Marguerite, Meignin, Véronique, Noguera, Maria-Elena, Harel, Stéphanie, and Arnulf, Bertrand

Abstract

Copyright of Hematologie is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2017
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17. Long-term follow-up analysis of 100 patients with splenic marginal zone lymphoma treated with splenectomy as first-line treatment

Author

Lenglet, Julien, primary, Traullé, Catherine, additional, Mounier, Nicolas, additional, Benet, Claire, additional, Munoz-Bongrand, Nicolas, additional, Amorin, Sandy, additional, Noguera, Maria-Elena, additional, Traverse-Glehen, Alexandra, additional, Ffrench, Martine, additional, Baseggio, Lucile, additional, Felman, Pascale, additional, Callet-Bauchu, Evelyne, additional, Brice, Pauline, additional, Berger, Françoise, additional, Salles, Gilles, additional, Brière, Josette, additional, Coiffier, Bertrand, additional, and Thieblemont, Catherine, additional

Published
2014
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18. NRAS:BCL-2 Complex Localization Determines Anti-Apoptotic Features Associated with Progressive Disease in Myelodysplastic Syndromes (MDS)

Author

Padua, Rose Ann, primary, Le Pogam, Carole, additional, Krief, Patricia, additional, Beurlet, Stephanie, additional, Cassinat, Bruno, additional, Cavé, Hélène, additional, Kosmider, Olivier, additional, Setterblad, Niclas, additional, Leboeuf, Christophe, additional, Sarda-Mantel, Laure, additional, Hervatin, Florence, additional, Merlet, Pascal, additional, Noguera, Maria-Elena, additional, Janin, Anne, additional, Pla, Marika, additional, Fontenay, Michaela, additional, Ades, Lionel, additional, Fenaux, Pierre, additional, Chomienne, Christine, additional, and Omidvar, Nader, additional

Published
2012
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19. BCL-2 Inhibition with ABT-737 Prolongs Survival in an NRAS/BCL2-Mediated MOUSE MODEL of Myelodyspastic Syndrome (MDS) Progressing to ACUTE Myelogenous Leukemia (AML) by Targeting Leukemia Initiating CELLS

Author

Pierre Fenaux, Michael Andreeff, Marina Konopleva, Beurlet Stephanie, Anne Janin, West Robert, Pierre de la Grange, Le Pogam Carole, Leboeuf Christophe, Krief Patricia, Rose Ann Padua, Petra Gorombei, Nader Omidvar, Noguera Maria-Elena, Christine Chomienne, and Pla Marika

Subjects
Genetically modified mouse, education.field_of_study, TUNEL assay, Acute myelogenous leukemia (AML), business.industry, Immunology, Population, Cell Biology, Hematology, medicine.disease, Biochemistry, Leukemia, medicine.anatomical_structure, Terminal deoxynucleotidyl transferase, Apoptosis, Cancer research, medicine, Bone marrow, education, business
Abstract

Abstract 678 Background and aims: BCL-2 activation plays a role in the progression of MDS to AML and BCL 2 inhibition may represent a therapeutic target in such patients. Using our double transgenic mouse model MRP8[NRASD12/BCL2], in which the transgenes induce MDS progressing to AML with dysplasia (Omidvar Cancer Res, 2007), we assessed the effect of ABT-737, a small molecule and mimetic inhibitor binding the BH3 domain of the BCL-2 family of proteins, on survival and leukemia initiating cells (LIC) in this mouse model. Methods: In this MRP8[NRASD12/hBCL2] double transgenic mouse model 2-week old mice have MDS with a mean of 6% bone marrow (BM) blasts (compared with 3% in the normal wild type littermates), while adult mice have AML, with a mean of 60% marrow blasts. In the present study, double transgenic mice were treated just after weaning and genotyping at 3 weeks of age with 75 mg/kg dose of ABT-737 (MDA & Abbott) 3 times weekly for 30 days. A cohort of mice (60 untreated and 35 treated) was followed for survival. Mice were sacrificed and BM harvested after treatment and Giemsa stained for BM analysis by microscopy (n=6 in each group), for LICs characterized as part of the lineage negative (Lin-)/Sca1+/cKit+ (LSK) population by flow cytometry (in 8 treated and 12 untreated mice), and for progenitor assays (n=4 in each group). Hematoxylin and eosin stained liver sections were examined and apoptosis assessed by the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assays of liver sections (n=4 per group). RNA was extracted from Sca+ enriched spleen cells from untreated and treated mice (n=3 from each group) and assayed for gene expression profiling using exon specific arrays (Affymetrix). Results: Survival from birth of 35 treated mice was significantly longer than for 60 untreated mice (p Conclusions: ABT-737 extends lifespan in NRASD12/BCL2 transgenic mice, a preclinical model of high risk MDS/AML. ABT-737 targets the leukemia initiating cell, and regulates, amongst several, cell cycle (proliferation), differentiation and apoptosis pathways. These data suggest that clinical trials in high risk MDS and AML patients are warranted. Disclosures: Grange: Genosplice Technology: Employment.

Published
2012

20. Normal levels of peripheral CD19+CD5+ CLL-like cells: Toward a defined threshold for CLL follow-up-A GEIL-GOELAMS study

Author

Durrieu, Françoise, primary, Geneviève, Franck, additional, Arnoulet, Christine, additional, Brumpt, Caren, additional, Capiod, Jean-Claude, additional, Degenne, Michel, additional, Feuillard, Jean, additional, Garand, Richard, additional, Kara-Terki, Amina, additional, Kulhein, Emilienne, additional, Maynadié, Marc, additional, Ochoa-Noguera, Maria-Elena, additional, Plesa, Adriana, additional, Roussel, Mikael, additional, Eghbali, Houchingue, additional, Truchan-Graczyk, Matgorzata, additional, de Carvalho Bittencourt, Marcelo, additional, Feugier, Pierre, additional, and Béné, Marie C., additional

Published
2011
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22. ABT-737 Targets Leukemic Stem Cells In Mouse Models of Mutant NRASD12/hBCL-2- Mediated Acute Myeloid Leukemia Progression with Increased Survival

Author

Padua, Rose Ann, primary, Beurlet, Stephanie, additional, Krief, Patricia, additional, Omidvar, Nader, additional, Pogam, Carole Le, additional, Auboeuf, Didier, additional, de la Grange, Pierre, additional, Soulie, Annie, additional, Janin, Anne, additional, Noguera, Maria-Elena, additional, Merlet, Pascal, additional, Sarda-Mantel, Laure, additional, Fenaux, Pierre, additional, Konopleva, Marina, additional, Andreeff, Michael, additional, Tu, Andrea, additional, Yang, Phoebe, additional, Fan, Alice C., additional, Kogan, Scott C., additional, Weissman, Irving L., additional, Felsher, Dean W., additional, Pla, Marika, additional, West, Robert, additional, and Chomienne, Christine, additional

Published
2010
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23. Mutant BCL2 Co-Operates with CBFβ/PEBP2β-MYH11 to Promote Expansion of Leukemia Initiating Cells with a Predominantly Pro-Apoptotic Mechanism Via Recruitment of Ras-GTP In a Mouse Model of Progressive Acute Myeloid Leukemia.

Author

Omidvar, Nader, primary, Pogam, Carole Le, additional, Beurlet, Stephanie, additional, Noguera, Maria-Elena, additional, Janin, Ann, additional, Kogan, Scott C., additional, Weissman, Irving L., additional, Pla, Marika, additional, Chomienne, Christine, additional, and Padua, Rose Ann, additional

Published
2010
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24. DNA Vaccination and All-Trans Retinoic Acid Treatment-Induced Long Term Survival Requires CD4+ and CD8+ T-Cell Activation in An APL Mouse Model.

Author

Padua, Rose Ann, primary, Furugaki, Kouichi, additional, Moins-Teisserenc, Helene, additional, Pokorna, Katerina, additional, Le Pogam, Carole, additional, Reboul, Murielle, additional, Aoki, Masayuki, additional, Bajzik, Veronique, additional, Krief, Patricia, additional, Janin, Anne, additional, Noguera, Maria-Elena, additional, West, Robert, additional, Schlageter, Marie-Helene, additional, Charron, Dominique, additional, Pla, Marika, additional, and Chomienne, Christine, additional

Published
2008
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25. ABT-737 Targets Intrinsic Apoptosis during Cooperation of BCL-2 and Oncogenic NRAS in An in Vivo Progression Model of Myelodysplasia/Acute Myeloid Leukaemia

Author

Omidvar, Nader, primary, Beurlet, Stephanie, additional, Le Pogam, Carole, additional, Janin, Anne, additional, Leboeuf, Christophe, additional, Soulie, Annie, additional, Setterblad, Niclas, additional, Noguera, Maria-Elena, additional, Sarda-Mantel, Laure, additional, Merlet, Pascal, additional, Pla, Marika, additional, Kogan, Scott C., additional, Weissman, Irving L, additional, Konopleva, Marina, additional, Bormann, William, additional, Andreeff, Michael, additional, Chomienne, Christine, additional, and Padua, Rose Ann, additional

Published
2008
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26. BCL-2 and Mutant NRAS Interact Physically and Functionally in a Mouse Model of Progressive Myelodysplasia

Author

Omidvar, Nader, primary, Kogan, Scott, additional, Beurlet, Stephanie, additional, le Pogam, Carole, additional, Janin, Anne, additional, West, Robert, additional, Noguera, Maria-Elena, additional, Reboul, Murielle, additional, Soulie, Annie, additional, Leboeuf, Christophe, additional, Setterblad, Niclas, additional, Felsher, Dean, additional, Lagasse, Eric, additional, Mohamedali, Azim, additional, Thomas, N. Shaun B., additional, Fenaux, Pierre, additional, Fontenay, Michaela, additional, Pla, Marika, additional, Mufti, Ghulam J., additional, Weissman, Irving, additional, Chomienne, Christine, additional, and Padua, Rose Ann, additional

Published
2007
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31. Cytogenetic studies on 519 consecutive de novo acute nonlymphocytic leukemias

Author

Berger, Roland, primary, Flandrin, Georges, additional, Bernheim, Alain, additional, Le Coniat, Maryvonne, additional, Vecchione, Danièle, additional, Pacot, Annie, additional, Derré, Josette, additional, Daniel, Marie-Thérèse, additional, Valensi, Françoise, additional, Sigaux, François, additional, and Ochoa-Noguera, Maria Elena, additional

Published
1987
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32. ABT-737 Targets Intrinsic Apoptosis during Cooperation of BCL-2 and Oncogenic NRAS in An in VivoProgression Model of Myelodysplasia/Acute Myeloid Leukaemia

Author

Omidvar, Nader, Beurlet, Stephanie, Le Pogam, Carole, Janin, Anne, Leboeuf, Christophe, Soulie, Annie, Setterblad, Niclas, Noguera, Maria-Elena, Sarda-Mantel, Laure, Merlet, Pascal, Pla, Marika, Kogan, Scott C., Weissman, Irving L, Konopleva, Marina, Bormann, William, Andreeff, Michael, Chomienne, Christine, and Padua, Rose Ann

Abstract

OBJECTIVES: Activating RAS mutations and over-expression of BCL-2 are prognostic features of myelodysplastic syndromes/acute myeloid leukemia (MDS/AML) transformation. Using NRASD12 and BCL-2, we created two distinct transplantable in vivomodels of MDS and AML. Expression of hBCL-2 in a primitive compartment by MMTV-LTR results in a disease resembling human MDS with bone marrow blasts of 15% with increased apoptosis assayed by TUNEL on liver sections, whilst the myeloid MRP8 promoter induces a disease with characteristics of human AML with marrow blasts of up to 90% with liver apoptosis patterns similar to wild type. In MDS mice RAS and BCL-2 do not co-localize in the mitochondria, but localize to the plasma membrane, where active pro-apoptotic RAS is normally located, whereas in the AML disease RAS and BCL-2 co-localize in the mitochondria, where BCL-2 is normally found; consistent with its anti-apoptotic properties. We next examine the mouse hematopoietic FDCP-1 in vitromodel with stable exogenous expression of NRASD12, hBCL-2 or NRASD12 and hBCL-2. Furthermore, we report the in vivoeffects of the BH-3 mimetic inhibitor ABT-737.

Published
2008
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33. Spontaneous abrogation of the G₂DNA damage checkpoint has clinical benefits but promotes leukemogenesis in Fanconi anemia patients.

Author

Ceccaldi, Raphael, Briot, Delphine, Larghero, Jérôme, Vasquez, Nadia, d'Enghien, Catherine Dubois, Chamousset, Deiphine, Noguera, Maria-Elena, Waisfisz, Quinten, Hermine, Olivier, Pondarre, Corinne, Leblanc, Thierry, Gluckman, Eliane, Joenje, Hans, Stoppa-Lyonnet, Dominique, Socié, Gerard, Soulier, Jean, Larghero, Jérôme, Dubois d'Enghien, Catherine, Chamousset, Delphine, and Socié, Gérard

Subjects
*DNA, *CELL cycle, *DISEASE progression, *FANCONI'S anemia, *BONE marrow, *CELL death, *CANCER treatment, *PROTEIN metabolism, *APLASTIC anemia, *BIOLOGICAL models, *CELL physiology, *COMPARATIVE studies, *GENETIC polymorphisms, *RESEARCH methodology, *MEDICAL cooperation, *GENETIC mutation, *MYELODYSPLASTIC syndromes, *NUCLEOTIDES, *PROTEIN kinases, *PROTEOLYTIC enzymes, *RESEARCH, *RNA, *TRANSFERASES, *PHENOTYPES, *EVALUATION research, *ACUTE myeloid leukemia, *DISEASE complications
Abstract

DNA damage checkpoints in the cell cycle may be important barriers against cancer progression in human cells. Fanconi anemia (FA) is an inherited DNA instability disorder that is associated with bone marrow failure and a strong predisposition to cancer. Although FA cells experience constitutive chromosomal breaks, cell cycle arrest at the G2 DNA damage checkpoint, and an excess of cell death, some patients do become clinically stable, and the mechanisms underlying this, other than spontaneous reversion of the disease-causing mutation, are not well understood. Here we have defined a clonal phenotype, termed attenuation, in which FA patients acquire an abrogation of the G2 checkpoint arrest. Attenuated cells expressed lower levels of CHK1 (also known as CHEK1) and p53. The attenuation could be recapitulated by modulating the ATR/CHK1 pathway, and CHK1 inhibition protected FA cells from cell death. FA patients who expressed the attenuated phenotype had mild bone marrow deficiency and reached adulthood, but several of them eventually developed myelodysplasia or leukemia. Better understanding of attenuation might help predict a patient's clinical course and guide choice of treatment. Our results also highlight the importance of evaluating the cellular DNA damage checkpoint and repair pathways in cancer therapies in general. [ABSTRACT FROM AUTHOR]

Published
2011
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34. Normal levels of peripheral CD19(+) CD5(+) CLL-like cells: toward a defined threshold for CLL follow-up -- a GEIL-GOELAMS study.

Author

Durrieu F, Geneviève F, Arnoulet C, Brumpt C, Capiod JC, Degenne M, Feuillard J, Garand R, Kara-Terki A, Kulhein E, Maynadié M, Ochoa-Noguera ME, Plesa A, Roussel M, Eghbali H, Truchan-Graczyk M, de Carvalho Bittencourt M, Feugier P, and Béné MC

Subjects
Adult, Aged, Aged, 80 and over, Antigens, CD19 blood, Antigens, CD19 immunology, CD5 Antigens blood, CD5 Antigens immunology, Cyclophosphamide therapeutic use, Female, Flow Cytometry, Follow-Up Studies, Humans, Leukemia, Lymphocytic, Chronic, B-Cell blood, Leukemia, Lymphocytic, Chronic, B-Cell diagnosis, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy, Leukemia, Lymphocytic, Chronic, B-Cell immunology, Lymphocyte Count, Male, Middle Aged, Neoplasm, Residual blood, Neoplasm, Residual immunology, ROC Curve, Reference Values, Sensitivity and Specificity, Vidarabine analogs & derivatives, Vidarabine therapeutic use, B-Lymphocytes chemistry, Immunophenotyping standards, Neoplasm, Residual diagnosis
Abstract

Background: The development of flow cytometry as a useful tool for the detection of minimal residual disease (MRD) in chronic lymphocytic leukemia (CLL) is potentially hampered by the fact that a normal subset of B-cells with a similar immunophenotype is present in the peripheral blood. This subset of CLL-like cells is not well defined in terms of frequency., Methods: Here, we performed a multicenter study with a panel of four-color antibody combinations possibly useful for the detection of MRD in CLL, to establish the levels of normal CLL-like cells in 49 healthy controls. ROC curves established the upper level of such cells at 4 × 10(-4) . The two best combinations were further applied to 419 samples from 117 treated CLL patients., Results: The combinations CD19/CD5/CD43/CD79b and CD19/CD5/CD81/CD22 appeared very robust and well correlated to enumerate normal CLL-like cells in a lysis no-wash approach. In follow-up samples from CLL patients, they disclosed only 9.8% of the samples within the normal range. In more than 90% of the cases, it was thus possible to report confidently on the absence or presence of MRD in these patients., Conclusions: This manuscript reports on the frequency of CD19(+) CD5(+) B-cells in normal peripheral blood and confirms the combinations recommended by the European research initiative on CLL as being performing to assess remaining CLL cells above a threshold of 4 × 10(-4) white blood cells., (2011 International Clinical Cytometry Society.)

Published
2011
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35. Mutual benefits of B-ALL and HLDA/HCDM HLDA 9th Barcelona 2010.

Author

Faure GC, Amsellem S, Arnoulet C, Bardet V, Campos L, De Carvalho-Bittencourt M, de Labarthe A, Eischen A, Feuillard J, Fossat C, Ottou FG, Guérin E, Guy J, Jouault H, Kuhlein E, Lacombe F, Lainey E, Maynadié M, Noguera ME, Roussel M, Solly F, Ballon OW, and Béné MC

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal immunology, Child, Child, Preschool, Gene Expression Regulation immunology, Humans, Infant, Middle Aged, Young Adult, Antigens, CD immunology, Gene Expression Profiling, Immunophenotyping, Precursor Cell Lymphoblastic Leukemia-Lymphoma immunology
Abstract

The B-cell panel of the ninth HLDA was applied in a multicentre fashion to cryopreserved cells from 46 patients with acute lymphoblastic leukemia. The reagents were aliquoted and shipped to volunteer participants from the French Groupe d'Etude Immunologique des Leucémies (GEIL). All samples were tested in flow cytometry, and the results collected as of the strength of labeling of the leukemic clone as negative, weak or strong. Among the 64 antibodies tested, the strongest and most frequent staining was observed for CD305 (LAIR), CD229 (Ly9), CD200 (OX-2) and, to a lesser extent, CD361 (EVI2b). Details of the observations, and information about the molecules tested are provided in the manuscript as well as a summary table., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Published
2011
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36. ZAP-70 protein expression and CD38 positivity in B-cell chronic lymphocytic leukemia.

Author

Ertault-Daneshpouy M, Noguera ME, Gisselbrecht C, Haddad A, Brice P, Marolleau JP, Soulier J, and Mounier N

Subjects
B-Lymphocyte Subsets classification, Biomarkers blood, Female, Humans, Immunophenotyping, Leukemia, Lymphocytic, Chronic, B-Cell classification, Male, Middle Aged, Prognosis, Retrospective Studies, ADP-ribosyl Cyclase 1 metabolism, B-Lymphocyte Subsets metabolism, Leukemia, Lymphocytic, Chronic, B-Cell metabolism, Membrane Glycoproteins metabolism, ZAP-70 Protein-Tyrosine Kinase metabolism
Abstract

Background: The clinical course, disease progression, and survival of B-cell chronic lymphocytic leukemia (B-CLL) have been correlated with immunoglobulin heavy-chain variable region mutation status. The biologic parameters 70-kDa zeta-associated protein (ZAP-70) and CD38 expression are easier and faster surrogate markers for mutational status., Objective: To assess retrospectively ZAP-70 expression in B-CLL cells using flow cytometry and examine its relationship with CD38 expression and the median time from diagnosis to initial therapy., Methods: Ninety-four unselected patients who had their follow-up in the outpatient clinic from 2004 to 2005 were reviewed for immunophenotyping ZAP-70 and CD38 expression. Direct immunolabeling with clone 2E3.2, isotype IgG2a, enabled easy quantification of ZAP-70 by flow cytometry in association with CD38 expression; in addition, the mean fluorescence intensity ratio (MFIR) of CD19+CD5+ B-CLL cells compared to an isotype control monoclonal antibody was determined., Results: ZAP-70 expression levels in B-CLL cells varied widely (0.3-99%). The median time to therapy was significantly shorter for the 54 patients with 20% or more ZAP-70+ cells (30 months) than for the 40 patients with less than 20% ZAP-70+ cells (median time to treatment not reached). The optimal MFIR for classifying patients as ZAP-70+ was 2. Thirty-two patients had a threshold of ZAP-70+CD38+ greater than 30%, with a median time from diagnosis to treatment of 19 months. Regardless of CD38 expression level, CD38 and ZAP-70 expressions were significantly associated. The median interval from diagnosis to initial therapy was 16.2 months for ZAP-70+CD38+ patients, 60 months for ZAP-70+CD38- or ZAP-70-CD38+ patients, and had not yet been reached for ZAP-70-CD38- patients., Conclusion: The association of ZAP-70+CD19+CD5+ B-CLL cells and percentage of CD38+CD19+CD5+ B-CLL cells evaluated by flow cytometry provide reliable methods that could be introduced into a routine diagnostic B-CLL panel to predict outcome.

Published
2008

37. Telehematology: a pilot experience of cytological diagnosis of acute myeloid leukemia via the Internet. A GOELAMS study.

Author

Leymarie V, Flandrin G, Noguera ME, Leymarie F, Lioure B, and Daliphard S

Subjects
Acute Disease, Cytological Techniques, Hematology methods, Humans, Pilot Projects, Internet, Leukemia, Myeloid diagnosis, Telemedicine
Abstract

Although modern communication technology is well developed, telehematology does not readily lend itself to practical laboratory use. Multicenter therapeutic protocols may offer preferential opportunities. The cytologists of the AML-2001 protocol established an innovative organization to demonstrate the reliability of the diagnostic assessment of acute myeloid leukemia through a rapid and decentralized exchange of information via the internet and to define the conditions optimizing expert diagnosis. Telediagnosis appears to be a powerful tool for cytological review and other issues.

Published
2006

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