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1. Prognostic value of multicenter flow cytometry harmonized assessment of minimal residual disease in acute myeloblastic leukemia

Author

Jean Feuillard, Florent Dumezy, Estelle Guérin, Kaoutar Allou, Marc Maynadié, André Baruchel, Christine Arnoulet, Francis Lacombe, Marie C. Béné, Orianne Wagner Ballon, Hélène Jouault, Groupe d'Etude Immunologique des Leucémies, Françoise Solly, Adrienne Delabarthe, Julien Guy, Lydia Campos, Norbert Ifrah, Pascale Lepelley, Hervé Dombret, Franck Geneviève, Claude Preudhomme, Service d'Hématologie [Bordeaux], CHU Bordeaux [Bordeaux], Hématologie de liaison avec Institut de Cancérologie de la Loire [CHU de Saint-Etienne], CHU Saint-Etienne, Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Service d'hématologie adulte [Hôpital de Saint Louis], CHU Saint Louis [APHP], Service d'Hématologie Cellulaire [Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Service d'Hématologie biologique [CHU Limoges], CHU Limoges, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Service d'hématologie biologique (CHU de Dijon), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Service d'Hématologie Biologique [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor, Service d'Hématologie Biologique [Hôpital Robert Debré, Paris], AP-HP Hôpital universitaire Robert-Debré [Paris], Hôpital Saint-Louis, Université Paris Diderot - Paris 7 (UPD7)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Laboratoire d'Hématologie Biologique (Hémato - ANGERS), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Service d'Hématologie [Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Hématologie Biologique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Registre des hémopathies malignes de Côte d'Or, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor, Service d'hématologie pédiatrique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service d'hématologie-oncologie adultes, Hematology Department, Université d'Angers (UA), Service d'Hématologie Clinique [Hôtel Dieu, Nantes], Hôtel-Dieu de Nantes, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], and Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)

Subjects
Male, Oncology, Cancer Research, Neoplasm, Residual, CD33, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], 0302 clinical medicine, Risk groups, AML, hemic and lymphatic diseases, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Prospective Studies, Child, Prospective cohort study, ComputingMilieux_MISCELLANEOUS, Boolean gates, medicine.diagnostic_test, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Hematology, General Medicine, Middle Aged, Prognosis, 3. Good health, Leukemia, Myeloid, Acute, MRD, [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, Child, Preschool, 030220 oncology & carcinogenesis, Female, Good prognosis, Adult, medicine.medical_specialty, Adolescent, Acute myeloblastic leukemia, [SDV.CAN]Life Sciences [q-bio]/Cancer, survival, Disease-Free Survival, Immunophenotyping, Flow cytometry, Young Adult, 03 medical and health sciences, Internal medicine, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], medicine, Humans, Time point, Aged, business.industry, flow cytometry, Infant, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, medicine.disease, Minimal residual disease, body regions, business, 030215 immunology
Abstract

IF 3.118; International audience; The assessment of minimal residual disease (MRD) in acute myeloblastic leukemia is of growing interest as a prognostic marker of patients' outcome. Multiparameter flow cytometry (MFC), tracking leukemia-associated immunophenotypic patterns, has been shown in several studies to be a useful tool to investigate MRD. Here, we report a multicenter prospective study which allowed to define a harmonized analysis strategy, as well as the efficacy of MFC MRD to predict outcome. This study included 276 patients, in 10 different MFC centers, of whom 268 had at least 1 MRD check point. The combination of a CD45, CD34, and CD33 backbone, with the addition of CD117, CD13, CD7, and CD15 in 2 five-color tubes allowed to define each patient's multiparameter immunophenotypic characteristics at diagnosis, according to a Boolean combination of gates. The same individual diagnosis gating strategy was then applied at each MRD time point for each patient. MRD levels were stratified according to log by log thresholds, from 5 × 10-2 (the classical morphological threshold to define remission) down to

Published
2018
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2. Erythrocyte density in sickle cell syndromes is associated with specific clinical manifestations and hemolysis

Author

Carlo Brugnara, Armando Teixeira-Pinto, Kamran Moradkhani, Pablo Bartolucci, Serge Pissard, Frédéric Galactéros, Hélène Jouault, Service de Médecine Interne [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre de référence des syndromes drépanocytaires majeurs, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Department of Laboratory Medicine, Boston Children's Hospital, Department of Biostatistics and Medical Informatics, Faculty of Medicine of Porto University, Service de Biochimie [Mondor], Service d'Hématologie Biologique [Mondor], and Guellaen, Georges

Subjects
Male, Pathology, Hemoglobin, Sickle, Hematocrit, Biochemistry, Gastroenterology, Hydroxycarbamide, Cohort Studies, chemistry.chemical_compound, 0302 clinical medicine, Medicine, Renal Insufficiency, Fetal Hemoglobin, 0303 health sciences, medicine.diagnostic_test, Hematology, Middle Aged, Hemolysis, Sickle cell anemia, 3. Good health, 030220 oncology & carcinogenesis, Female, medicine.drug, Adult, medicine.medical_specialty, Immunology, Erythrocytes, Abnormal, Anemia, Sickle Cell, 03 medical and health sciences, Young Adult, alpha-Thalassemia, Internal medicine, Lactate dehydrogenase, Fetal hemoglobin, Skin Ulcer, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Priapism, 030304 developmental biology, Aged, Biologic marker, Red Cell, L-Lactate Dehydrogenase, business.industry, Bilirubin, Cell Biology, medicine.disease, chemistry, business
Abstract

Dense, dehydrated red blood cells (DRBCs) are a characteristic feature of sickle-cell disease (SCD). DRBCs play a role in the pathophysiology of SCD acute and chronic organ damage because of heightened tendency to undergo polymerization and sickling because of their higher hemoglobin S concentration. Relations between red cell density (assessed with phthalate density-distribution profile method) and several hematologic, biochemical, genetic parameters, and clinical manifestations were studied in a large cohort of homozygous patients. The percentage of DRBCs was significantly higher in patients who experienced skin ulcers, priapism, or renal dysfunction. Presence of α-thalassemia deletions was associated with fewer DRBCs. A multivariable analysis model showed DRBCs to be positively associated with hemolytic parameters such as lactate dehydrogenase and bilirubin and negatively with fetal hemoglobin. The percentage of DRBCs decreased by 34% at 6 months of hydroxycarbamide (xydroxyurea) therapy. Thus, DRBCs are associated with specific clinical manifestations and biologic markers and may be a useful addition to the biologic and clinical evaluation of patients with SCD, because they can easily be measured in a hematocrit tube.

Published
2012
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3. h-Goliath, paralog of GRAIL, is a new E3 ligase protein, expressed in human leukocytes

Author

Frédérique Bulle, Georges Guellaen, Adeline Guais, S. Siegrist, Brigitte Solhonne, Hélène Jouault, Remodelage Tissulaire et Fibrose, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Cochin (UMR_S567 / UMR 8104), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5), Biochimie cellulaire : relations cycle cellulaire, cytosquelette et traduction (BCRCCCT), Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC), Unité de Recherche en Epidémiologie Nutritionnelle (UREN), Université Paris 13 (UP13)-Institut National de la Recherche Agronomique (INRA)-Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'Hématologie Biologique, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), We thank Hélène Nuyttens for her technical assistance. Adeline Guais is a recipient of a grant from the Ministère de la Recherche et de la Technologie. This work was financially supported by the Institut National de la Santé et de la Recherche Médicale. We thank Fanny Brizzy for critical reading of the manuscript., Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Université Paris 13 (UP13)-Institut National de la Recherche Agronomique (INRA)-Conservatoire National des Arts et Métiers [CNAM] (CNAM), HESAM Université - Communauté d'universités et d'établissements Hautes écoles Sorbonne Arts et métiers université (HESAM)-HESAM Université - Communauté d'universités et d'établissements Hautes écoles Sorbonne Arts et métiers université (HESAM)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Institut Cochin ( UMR_S567 / UMR 8104 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Biochimie cellulaire : relations cycle cellulaire, cytosquelette et traduction ( BCRCCCT ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Centre National de la Recherche Scientifique ( CNRS ), Unité de Recherche en Epidémiologie Nutritionnelle ( UREN ), Université Paris 13 ( UP13 ) -Institut National de la Recherche Agronomique ( INRA ) -Conservatoire National des Arts et Métiers [CNAM] ( CNAM ) -Université Sorbonne Paris Cité ( USPC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), and Guellaen, Georges

Subjects
Gene isoform, Ubiquitin-Protein Ligases, Amino Acid Motifs, Molecular Sequence Data, Gene Expression, Protein Sorting Signals, Biology, 03 medical and health sciences, DDB1, 0302 clinical medicine, Ubiquitin, Complementary DNA, [SDV.BDD] Life Sciences [q-bio]/Development Biology, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Leukocytes, Genetics, Humans, Tissue Distribution, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [ SDV.BDD ] Life Sciences [q-bio]/Development Biology, Amino Acid Sequence, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Transcription factor, Gene, [SDV.BDD]Life Sciences [q-bio]/Development Biology, 030304 developmental biology, 0303 health sciences, Base Sequence, Sequence Homology, Amino Acid, General Medicine, Immunohistochemistry, Molecular biology, Protein Structure, Tertiary, Ubiquitin ligase, Molecular Weight, 030220 oncology & carcinogenesis, Mesoderm formation, biology.protein, Hydrophobic and Hydrophilic Interactions
Abstract

In Drosophila, the RING finger protein d-Goliath was originally identified as a transcription factor involved in the embryo mesoderm formation [Bouchard, M.L., Cote, S., 1993. The Drosophila melanogaster developmental gene g1 encodes a variant zinc-finger-motif protein. Gene 125, 205-209]. In mouse, the m-Goliath mRNA level was shown to be increased in growth factor withdrawal-induced apoptosis of myeloid cells [Baker, S.J., Reddy, E.P., 2000. Cloning of murine G1RP, a novel gene related to Drosophila melanogaster g1. Gene 248, 33-40]. Due to its putative function of transcription factor in apoptosis, we cloned the human cDNA for h-Goliath and characterized the expression of the protein in blood and bone marrow cells. The human protein of 419 aa (44 kDa) contains a protease-associated domain, a transmembrane domain and a RING-H2 motif. This structure classifies h-Goliath as a new member of a human family of ubiquitin ligases with GRAIL (gene related to anergy in lymphocytes) as founder. This E3 ligase controls the development of T cell clonal anergy by ubiquitination [Anandasabapathy, N., Ford, G.S., Bloom, D., Holness, C., Paragas, V., Seroogy, C., Skrenta, H., Hollenhorst, M., Fathman, C.G., Soares, L., 2003. GRAIL: an E3 ubiquitin ligase that inhibits cytokine gene transcription is expressed in anergic CD4+ T cells. Immunity 18, 535-547]. In vitro ubiquitination studies support the E3 ubiquitin ligase activity of h-Goliath. In human, the protein is expressed under 3 isoforms, a major one at 28 kDa and two others at 46 and 55 kDa. These proteins come from a common precursor (44 kDa) as we observed using in vitro transcription-translation. Using immunohistochemistry on blood or bone marrow smears, of healthy or leukemia samples, we found that the protein expression was restricted to the cytoplasm of progenitors and fully differentiated leukocyte populations. We did not observe any modification of h-Goliath expression or localization in leukemia. In these cells, this new E3 ubiquitin ligase protein does not seem associated with a differentiation state of the cell or with apoptosis.

Published
2006
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4. A mouse model provides evidence that genetic background modulates anemia and liver injury in erythropoietic protoporphyria

Author

Marie Abitbol, Jean-Louis Guénet, Hervé Puy, Hélène Jouault, Florence Bernex, Xavier Montagutelli, Jean-Charles Deybach, Génétique Moléculaire et Cellulaire (UGMC), École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), Génétique des Mammifères, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Centre Français des Porphyries Hôpital Louis Mourier, Université Paris Diderot - Paris 7 (UPD7), Institut Mondor de recherche biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Génétique fonctionnelle et médicale, Institut National de la Recherche Agronomique (INRA), Service d'Hématologie Biologique, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre Français des Porphyries, Hopital Louis Mourier - AP-HP [Colombes], Département de Biologie du Développement, Institut Pasteur [Paris], Génétique Fonctionnelle de la Souris, École nationale vétérinaire - Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), and Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, Physiology, [SDV]Life Sciences [q-bio], Protoporphyrins, Severity of Illness Index, Liver disease, chemistry.chemical_compound, Mice, 0302 clinical medicine, Animals, Congenic, Bone Marrow, ComputingMilieux_MISCELLANEOUS, Liver injury, PROTOPORPHYRIN, BILIRUBIN, CHRONIC HEPATITIS, FERROCHELATASE, CONGENIC STRAINS, BILIRUBINE, HEPATITE CHRONIQUE, LIGNEE CONGENIQUES, 0303 health sciences, Mice, Inbred BALB C, Gastroenterology, Anemia, Jaundice, Ferrochelatase, 3. Good health, Phenotype, 030220 oncology & carcinogenesis, Female, Erythropoietic protoporphyria, medicine.symptom, medicine.medical_specialty, Protoporphyria, Erythropoietic, Congenic, Biology, 03 medical and health sciences, Physiology (medical), Internal medicine, medicine, Animals, Humans, 030304 developmental biology, [SDV.GEN]Life Sciences [q-bio]/Genetics, Hepatology, medicine.disease, Mice, Inbred C57BL, Disease Models, Animal, [SDV.GEN.GA]Life Sciences [q-bio]/Genetics/Animal genetics, Endocrinology, chemistry, protoporphyrine, Immunology, Mutation, biology.protein, Protoporphyrin, Liver Failure, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Erythropoietic protoporphyria is an inherited disorder of heme biosynthesis caused by partial ferrochelatase deficiency, resulting in protoporphyrin (PP) overproduction by erythrocytes. In humans, it is responsible for painful skin photosensitivity and, occasionally, liver failure due to accumulation of PP in the liver. The ferrochelatase deficiency mouse mutation is the best animal model available for human erythropoietic protoporphyria. The original description, based on mice with a BALB/cByJCrl genetic background, reported a disease resembling the severe form of the human disease, with anemia, jaundice, and liver failure. Using congenic strains, we investigated the effect of genetic background on the severity of the phenotype. Compared with BALB/cByJCrl, C57BL/6JCrl mice developed moderate but increasing anemia and intense liver accumulation of PP with severe hepatocyte damage and loss. Bile excretory function was not affected, and bilirubin remained low. Despite the highest PP concentration in erythrocytes, anemia was mild and there were few PP deposits in the liver in SJL/JOrlCrl homozygotes. Discriminant analysis using six hematologic and biochemical parameters showed that homozygotes of the three genetic backgrounds could be clustered in three well-separated groups. These three congenic strains provide strong evidence for independent genetic control of bone marrow contribution of PP overproduction to development of liver disease and biliary PP excretion. They provide a tool to investigate the physiological mechanisms involved in these phenotypic differences and to identify modifying genes.

Published
2005
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