11 results on '"Willekens, Christophe"'
Search Results
2. Coopération entre les mutations Jak2 V617F et Srsf2 P95Hdans le système hématopoïétique
- Author
-
Willekens, Christophe and STAR, ABES
- Subjects
[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/Hematology ,SRSF2 ,JAK2 ,[SDV.CAN] Life Sciences [q-bio]/Cancer ,Signalisation ,Modèles murins ,Épissage ,Signalling ,Neoplasmes myéloprolifératifs ,Splicing ,Myeloproliferative neoplasms ,Mouse model - Abstract
JAK2 V617F mutation is frequently identified in myeloproliferative neoplasms (MPN). Additional somatic variants are supposed to contribute to bone marrow fibrosis or acute myeloid leukemia evolution. One of these mutations affects SRSF2, a gene encoding a component of the splicing machinery. To investigate how Jak2 V617F and Srsf2 P95H mutations interact in the hematopoietic tissue, we generated conditional knock-in mice in which the two mutations were expressed upon the control of Scl gene. Our study shows that Srsf2 P95H mutation initially exhibits limited effect on Jak2 V617F polycythemia and thrombocytosis but induces a delay in myelofibrosis development and protect hematopoietic stem cell from exhaustion observed after serial transplantation in Jak2 V617F single mutant cells. We focused on megakaryocyte (MK), implied in fibrosis development and found that Srsf2P95H partially reversed MKabnormalities induced by Jak2 V617F (cell size, normalized ploidy and expression of c-Mpl). Analysis of c-Mpl/Jak2 signaling with mass cytometry revealed a slight reduced proportion of MK expressing high levels of P-Stat5 in case of Srsf2 P95H co-occurrence with Jak2 V617F while treatment with high dose of the thrombopoietin-mimetic romiplostim in mice transplanted with wild-type or Srsf2 P95H bone marrow cells confirms the negative impact of Srsf2 P95H on fibrosis development. Gene expression analysis on sorted MK confirms down-regulation of Jak/Stat signaling pathway induced by Srsf2 P95H and reveals that Srsf2 P95H mutation more frequently induces exon 14 skipping of Jak2 mRNA. These result was confirmed in granulocytes samples from patients with JAK2 V617F MPN with associated SRSF2 P95H mutation., La mutation JAK2 V617F est fréquemment observée en cas de néoplasme myéloprolifératif (NMP). D’autres mutations somatiques peuvent être associées et sont corrélées au stade myélofibrotique ou à une évolution en leucémie aigüe. L’une de ces mutations touche le gène SRSF2, codant pour une protéine du complexe d’épissage. Pour étudier l’interaction entre les mutations Jak2 V617F et Srsf2 P95H dans le tissu hématopoïétique, nous avons généré un modèle murin knock-in conditionnel des deux mutations s’exprimant sous le contrôle du gène Scl. Notre étude montre que Srsf2 P95H limite peu le développement de la polyglobulie et de la thrombocytose induites par Jak2 V617F mais freine l’évolution vers une fibrose médullaire et protège les cellules souches hématopoïétiques de l’épuisement en transplantations sériées. L’étude des mégacaryocytes (MK), impliqués dans le processus fibrotique, montre que Srsf2 P95H induit une quasi-normalisation des anomalies induites par Jak2 V617F (taille, ploïdisation, expression de c-Mpl). L’analyse de la signalisation c-Mpl/Jak2 par cytométrie de masse révèle une discrète diminution de la proportion de MK exprimant de haut niveau de P-Stat5 en cas de mutation Srsf2 P95H associée à Jak2 V617F tandis que l’injection d’un agoniste de la thrombopoïetine à fortes doses confirme l’impact négatif de Srsf2 P95H sur le développement de la fibrose. L’étude de l’expression génique de MK triés confirme l’altération de la voie Jak/Stat induite par Srsf2 P95H et révèle que Srsf2 P95H induit plus fréquemment une perte de l’exon 14 (incluant la mutation V617F) de l’ARNm de Jak2. Ce résultat est confirmé sur des échantillons de granulocytes de patients atteints de NMP JAK2 V617F avec mutation SRSF2 P95H associée.
- Published
- 2021
3. First-in-Human Phase I Study of Iadademstat (ORY-1001): A First-in-Class Lysine-Specific Histone Demethylase 1A Inhibitor, in Relapsed or Refractory Acute Myeloid Leukemia
- Author
-
Salamero, Olga, Montesinos, Pau, Willekens, Christophe, Pérez-Simón, José Antonio, Pigneux, Arnaud, Récher, Christian, Popat, Rakesh, Carpio Segura, Cecilia del Carmen, Molinero, César, Mascaró, Cristina, Vila, Joaquim, Arévalo, M. Isabel, Maes, Tamara, Buesa, Carlos, Bosch José, Francesc Xavier, The University of Manchester, Universitat Autònoma de Barcelona, Institut Català de la Salut, [Salamero O, Carpio C, Bosch F] Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institute of Oncology (VHIO), Barcelona, Spain. Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain. [Montesinos P] Hospital Universitari I Politécnic La Fe, València, Spain. Centro de Investigación Biomédica en Red de Cáncer, Instituto Carlos III, Madrid, Spain. [Willekens C] Institut Gustave Roussy, Villejuif Cedex, France. [Pérez-Simón JA] Hospital Universitario Virgen del Rocío, Sevilla, Spain. Instituto de Biomedicina de Sevilla (Insitituto de Biomedicina De Sevilla/Consejo Superior De Investigaciones Científicas/Centro de Investigación Biomédica en Red de Cáncer), Universidad de Sevilla, Sevilla, Spain. [Pigneux A] Centre Hospitalier Universitaire CHU Bordeaux, Hôpital du Haut Lévêque, Pessac, France. [Récher C] Hospitalier Universitaire de Toulouse, Institut Universitaire du Cancer de Toulouse Oncopole, Université Toulouse III Paul Sabatier, Toulouse, France, Vall d'Hebron Barcelona Hospital Campus, Ministerio de Economía y Competitividad (España), European Commission, Cancer Research UK, Centro para el Desarrollo Tecnológico Industrial (España), National Institute for Health Research (UK), University College London, and NIHR Biomedical Research Centre (UK)
- Subjects
Adult ,Male ,Cancer Research ,Myeloid ,Lysine-Specific Histone Demethylase 1A ,acciones y usos químicos::acciones farmacológicas::mecanismos moleculares de acción farmacológica::inhibidores enzimáticos [COMPUESTOS QUÍMICOS Y DROGAS] ,neoplasias::neoplasias por tipo histológico::leucemia::leucemia mieloide::leucemia mieloide aguda [ENFERMEDADES] ,Refractory ,In vivo ,Recurrence ,hemic and lymphatic diseases ,medicine ,Hematologic Malignancy ,Humans ,Other subheadings::/therapeutic use [Other subheadings] ,Enzyme Inhibitors ,Aged ,Aged, 80 and over ,Histone Demethylases ,business.industry ,Leucèmia mieloide aguda ,Otros calificadores::/uso terapéutico [Otros calificadores] ,Myeloid leukemia ,Neoplasms::Neoplasms by Histologic Type::Leukemia::Leukemia, Myeloid::Leukemia, Myeloid, Acute [DISEASES] ,KDM1A ,ORIGINAL REPORTS ,Middle Aged ,medicine.disease ,In vitro ,Leukemia ,Leukemia, Myeloid, Acute ,medicine.anatomical_structure ,Oncology ,Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Enzyme Inhibitors [CHEMICALS AND DRUGS] ,Cancer research ,Female ,business ,Inhibidors enzimàtics - Ús terapèutic - Abstract
[Purpose] Iadademstat is a novel, highly potent, and selective inhibitor of LSD1 (KDM1A), with preclinical in vitro and in vivo antileukemic activity. This study aimed to determine safety and tolerability of iadademstat as monotherapy in patients with relapsed/refractory acute myeloid leukemia (R/R AML)., [Methods] This phase I, nonrandomized, open-label, dose-escalation (DE), and extension-cohort (EC) trial included patients with R/R AML and evaluated the safety, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary antileukemic activity of this orally bioavailable first-in-class lysine-specific demethylase 1 inhibitor., [Results] Twenty-seven patients were treated with iadademstat on days 1 to 5 (5-220 µg/m2/d) of each week in 28-day cycles in a DE phase that resulted in a recommended dose of 140 µg/m2/d of iadademstat as a single agent. This dose was chosen to treat all patients (n = 14) in an EC enriched with patients with MLL/KMT2A-rearranged AML. Most adverse events (AEs) were as expected in R/R AML and included myelosuppression and nonhematologic AEs, such as infections, asthenia, mucositis, and diarrhea. PK data demonstrated a dose-dependent increase in plasma exposure, and PD data confirmed a potent time- and exposure-dependent induction of differentiation biomarkers. Reductions in blood and bone marrow blast percentages were observed, together with induction of blast cell differentiation, in particular, in patients with MLL translocations. One complete remission with incomplete count recovery was observed in the DE arm., [Conclusion] Iadademstat exhibits a good safety profile together with signs of clinical and biologic activity as a single agent in patients with R/R AML. A phase II trial of iadademstat in combination with azacitidine is ongoing (EudraCT No.: 2018-000482-36)., Supported by Oryzon Genomics and IPT-2012-0673-010000 of the INNPACTO program of the Spanish Ministry of Economy and Competitiveness, with contribution of Fondo Europeo de Desarrollo Regional (FEDER) from the European Union and CDTI_CIIP-20131005/EUROSTAR_E18159. T.C.P.S. is supported by Cancer Research UK Grant No. C5759/A20971. R.P. is supported by the National Institute for Health Research, University College London Hospitals, Biomedical Research Centre.
- Published
- 2020
4. Characteristics and outcome of patients with low-/intermediate-risk acute promyelocytic leukemia treated with arsenic trioxide - an international collaborative study
- Author
-
Kayser, Sabine, Schlenk, Richard F., Lebon, Delphine, Carre, Martin, Götze, Katharina S., Stölzel, Friedrich, Berceanu, Ana, Schäfer-Eckart, Kerstin, Peterlin, Pierre, Hicheri, Yosr, Rahme, Ramy, Raffoux, Emmanuel, Chermat, Fatiha, Krause, Stefan W., Aulitzky, Walter E., Rigaudeau, Sophie, Noppeney, Richard, Berthon, Celine, Görner, Martin, Jost, Edgar, Carassou, Philippe, Keller, Ulrich, Orvain, Corentin, Braun, Thorsten, Saillard, Colombe, Arar, Ali, Kunzmann, Volker, Wemeau, Mathieu, De Wit, Maike, Niemann, Dirk, Bonmati, Caroline, Schwänen, Carsten, Abraham, Julie, Aljijakli, Ahmad, Haiat, Stephanie, Krämer, Alwin, Reichle, Albrecht, Gnadler, Martina, Willekens, Christophe, Spiekermann, Karsten, Hiddemann, Wolfgang, Müller-Tidow, Carsten, Thiede, Christian, Röllig, Christoph, Serve, Hubert, Bornhäuser, Martin, Baldus, Claudia D., Lengfelder, Eva, Fenaux, Pierre, Platzbecker, Uwe, and Adès, Lionel
- Subjects
ddc - Published
- 2020
5. Impact and consequences of intensive chemotherapy on intestinal barrier and microbiota in acute myeloid leukemia: the role of mucosal strengthening
- Author
-
Hueso, Thomas, Ekpe, Kenneth, Mayeur, Camille, Gatse, Anna, Joncquel-Chevallier Curt, Marie, Gricourt, Guillaume, Rodriguez, Christophe, Burdet, Charles, Ulmann, Guillaume, Neut, Christel, Amini, Salah-Eddine, Lepage, Patricia, Raynard, Bruno, Willekens, Christophe, Micol, Jean-Baptiste, de Botton, Stéphane, Yakoub-Agha, Ibrahim, Gottrand, Frédéric, Desseyn, Jean-Luc, Thomas, Muriel, Woerther, Paul-Louis, Seguy, David, Institute for Translational Research in Inflammation - U 1286 (INFINITE (Ex-Liric)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), AgroParisTech-Université Paris-Saclay-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre Hospitalier Universitaire de Lille (CHU Lille), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Emergence de la résistance bactérienne in vivo (EA3964), Université Paris Diderot - Paris 7 (UPD7), Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Département de cancérologie de l'enfant et de l'adolescent [Gustave Roussy], Institut Gustave Roussy (IGR), Département d’Innovation Thérapeutique et essais précoces [Gustave Roussy] (DITEP), Centre hospitalier universitaire Henri-Mondor [Créteil], Dynamic Microbiology - EA 7380 (DYNAMIC), École nationale vétérinaire - Alfort (ENVA)-Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES)-Université Paris-Est (UPE)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Service des Maladies de l'Appareil Digestif et de la Nutrition [CHRU Lille], Hôpital Claude Huriez [Lille], CHU Lille-CHU Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), University Hospital of Lille, MSD, École nationale vétérinaire d'Alfort (ENVA)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CHU Lille, and Tâche, Roselyne
- Subjects
Adult ,Male ,[SDV]Life Sciences [q-bio] ,Mice, Transgenic ,chemotherapy ,Feces ,Mice ,mucus ,Antineoplastic Combined Chemotherapy Protocols ,microbiota ,Animals ,Humans ,acute leukemia ,Intestinal Mucosa ,lcsh:RC799-869 ,Aged ,[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology ,Induction Chemotherapy ,Middle Aged ,Fatty Acids, Volatile ,Gastrointestinal Microbiome ,[SDV] Life Sciences [q-bio] ,Leukemia, Myeloid, Acute ,intestinal barrier ,Dysbiosis ,Female ,lcsh:Diseases of the digestive system. Gastroenterology ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology ,Research Article ,Research Paper - Abstract
International audience; Induction chemotherapy (7 + 3 regimen) remains the gold standard for patients with acute myeloid leukemia (AML) but is responsible for gut damage leading to several complications such as bloodstream infection (BSI). We aimed to investigate the impact of induction chemotherapy on the intestinal barrier of patients with AML and in wild-type mice. Next, we assessed the potential benefit of strengthening the mucosal barrier in transgenic mice releasing a recombinant protein able to reinforce the mucus layer (Tg222). In patients, we observed a decrease of plasma citrulline, which is a marker of the functional enterocyte mass, of short-chain fatty acids and of fecal bacterial load, except forEscherichia coliandEnterococcusspp., which became dominant. Both the alpha and beta-diversities of fecal microbiota decreased. In wild-type mice, citrulline levels decreased under chemotherapy along with an increase ofE. coliandEnterococcusspp load associated with concomitant histologic impairment. By comparison with wild-type mice, Tg222 mice, 3 days after completing chemotherapy, had higher citrulline levels, a faster healing epithelium, and preserved alpha-diversity of their intestinal microbiota. This was associated with reduced bacterial translocations. Our results highlight the intestinal damage and the dysbiosis induced by the 7 + 3 regimen. As a proof of concept, our transgenic model suggests that strengthening the intestinal barrier is a promising approach to limit BSI and improve AML patients' outcome.
- Published
- 2020
6. CHIP in the molecular landscape of TRMN
- Author
-
Hachem, Sabine Khalife, Saleh, Khalil, Pasquier, Florence, Tarabay, Anthony, Quivoron, Cyril, Cotteret, Sophie, Willekens, Christophe, Saada, Véronique, Ines-Maria Vaz-Luis, Delaloge, Suzette, Leary, Alexandra, Raslova, Hana, Rosselli, Filippo, Caron, Olivier, Iléana Antony-Debré, Solary, Eric, Botton, Stéphane De, Marzac, Christophe, and Jean-Baptiste Micol
- Published
- 2019
- Full Text
- View/download PDF
7. A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset
- Author
-
Selimoglu-Buet, Dorothée, Rivière, Julie, Ghamlouch, Hussein, Bencheikh, Laura, Lacout, Catherine, Morabito, Margot, Diop, M’boyba, Meurice, Guillaume, Breckler, Marie, Chauveau, Aurélie, Debord, Camille, Debeurme, Franck, Itzykson, Raphael, Chapuis, Nicolas, Willekens, Christophe, Wagner-Ballon, Orianne, Bernard, Olivier A., Droin, Nathalie, Solary, Eric, Hématopoïèse normale et pathologique (U1170 Inserm), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), Plateforme de Bioinformatique [Gustave Roussy], Analyse moléculaire, modélisation et imagerie de la maladie cancéreuse (AMMICa), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Etude du Polymorphisme des Génomes Végétaux (EPGV), Institut National de la Recherche Agronomique (INRA), Service d'Hématologie Biologique [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Thérapeutique Recombinante Expérimentale (TIMC-IMAG-TheREx), Techniques de l'Ingénierie Médicale et de la Complexité - Informatique, Mathématiques et Applications, Grenoble - UMR 5525 (TIMC-IMAG), Université Joseph Fourier - Grenoble 1 (UJF)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP)-IMAG-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA)-Université Joseph Fourier - Grenoble 1 (UJF)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP)-IMAG-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA), Hématopoïèse normale et pathologique, Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Direction des systèmes d'information, Ministére des Affaires Etrangères, Ministère de l'Europe et des Affaires étrangères (MEAE), Service d'Hématologie Clinique [CHU Lille], Hôpital Claude Huriez, CHU Henri Mondor, Université Paris-Sud 11 - Faculté de médecine (UP11 UFR Médecine), Centre de Recherches Juridiques de l'Université de Franche-Comté - UFC (EA 3225) (CRJFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université de Franche-Comté (UFC), Département d'hématologie [Gustave Roussy], and Institut Gustave Roussy (IGR)
- Subjects
Male ,Mice, Knockout ,Gene Expression Regulation, Leukemic ,Science ,Primary Cell Culture ,Down-Regulation ,Leukemia, Myelomonocytic, Chronic ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,DNA Methylation ,Article ,Monocytes ,Dioxygenases ,DNA-Binding Proteins ,Mice ,MicroRNAs ,Proto-Oncogene Proteins ,Animals ,Humans ,Female ,lcsh:Q ,K562 Cells ,Promoter Regions, Genetic ,lcsh:Science - Abstract
Non-classical monocyte subsets may derive from classical monocyte differentiation and the proportion of each subset is tightly controlled. Deregulation of this repartition is observed in diverse human diseases, including chronic myelomonocytic leukemia (CMML) in which non-classical monocyte numbers are significantly decreased relative to healthy controls. Here, we identify a down-regulation of hsa-miR-150 through methylation of a lineage-specific promoter in CMML monocytes. Mir150 knock-out mice demonstrate a cell-autonomous defect in non-classical monocytes. Our pulldown experiments point to Ten-Eleven-Translocation-3 (TET3) mRNA as a hsa-miR-150 target in classical human monocytes. We show that Tet3 knockout mice generate an increased number of non-classical monocytes. Our results identify the miR-150/TET3 axis as being involved in the generation of non-classical monocytes., A decrease in the fraction of non-classical monocytes is a hallmark of chronic myelomonocytic leukaemia. Taking advantage of this abnormal situation, the authors identify a mechanistic link between miR-150 and TET3 as being involved in monocyte subset generation.
- Published
- 2018
8. IDH1 and IDH2 mutations as novel therapeutic targets: current perspectives
- Author
-
de Botton, Stephane, Mondesir,Johanna, Willekens,Christophe, and Touat,Mehdi
- Subjects
Journal of Blood Medicine - Abstract
Johanna Mondesir1,2 Christophe Willekens3–5 Mehdi Touat6,7 Stéphane de Botton3–5 1Service d’Immunopathologie Clinique, Hôpital Saint Louis, 2CNRS UMR8104, INSERM U1016, Institut Cochin, Université Paris Descartes, Paris, 3Gustave Roussy, Université Paris-Saclay, Service d’Hématologie Clinique, 4INSERM U1170, Gustave Roussy, Université Paris-Saclay, Villejuif, 5Faculté de médecine Paris-Sud, Kremlin-Bicêtre, 6AP-HP, Hôpitaux Universitaires La Pitié Salpêtrière – Charles Foix, Service de Neurologie 2-Mazarin, Paris, 7Gustave Roussy, Université ParisâSaclay, Département d’Innovation Thérapeutique et d’Essais Précoces, Villejuif, France Abstract: Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are key metabolic enzymes that convert isocitrate to α-ketoglutarate. IDH1/2 mutations define distinct subsets of cancers, including low-grade gliomas and secondary glioblastomas, chondrosarcomas, intrahepatic cholangiocarcinomas, and hematologic malignancies. Somatic point mutations inIDH1/2confer a gain-of-function in cancer cells, resulting in the accumulation and secretion in vast excess of an oncometabolite, the D-2-hydroxyglutarate (D-2HG). Overproduction of D-2HG interferes with cellular metabolism and epigenetic regulation, contributing to oncogenesis. Indeed, high levels of D-2HG inhibit α-ketoglutarate-dependent dioxygenases, including histone and DNA demethylases, leading to histone and DNA hypermethylation and finally a block in cell differentiation. Furthermore, D-2HG is a biomarker suitable for the detection ofIDH1/2mutations at diagnosis and predictive of the clinical response. Finally, mutant-IDH1/2 enzymes inhibitors have entered clinical trials for patients withIDH1/2mutations and represent a novel drug class for targeted therapy. Keywords: tumor metabolism, epigenetic, oncogene, IDH1, IDH2, glioma, acute myeloid leukemia, 2-HG, targeted therapies
- Published
- 2016
9. Bendamustine and rituximab combination in the management of chronic lymphocytic leukemia-associated autoimmune hemolytic anemia: A multicentric retrospective study of the French CLL intergroup (GCFLLC/MW and GOELAMS)
- Author
-
Quinquenel, Anne, Willekens, Christophe, Dupuis, Jehan, Royer, Bruno, Ysebaert, Loic, Guibert, S. De, Michallet, Anne-Sophie, Feugier, Pierre, Guiéze, Romain, Levy, Vincent, Delmer, Alain, Service d'Hématologie Clinique [CHU Reims], Hôpital universitaire Robert Debré [Reims], Université de Reims Champagne-Ardenne (URCA), Service d'Hématologie Clinique [CHU Lille], Hôpital Claude Huriez [Lille], CHU Lille-CHU Lille, Service d'hématologie clinique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Laboratoire d'Hématologie [CHU Amiens], CHU Amiens-Picardie, Institut Universitaire du Cancer de Toulouse - Oncopole (IUCT Oncopole - UMR 1037), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Rennes (UR)-Hôpital Pontchaillou, Hématologie clinique, CHU Lyon, Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Nutrition-Génétique et Exposition aux Risques Environnementaux (NGERE), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), CHU Estaing [Clermont-Ferrand], CHU Clermont-Ferrand, Hôpital Avicenne [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Rennes 1 (UR1), and Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Hôpital Pontchaillou
- Subjects
immune system diseases ,hemic and lymphatic diseases ,[SDV]Life Sciences [q-bio] - Abstract
International audience; We report our experience on bendamustine and rituximab (BR) combination in 26 patients with chronic lymphocytic leukemia (CLL) complicated by autoimmune hemolytic anemia (AIHA). At the time of BR initiation, 88% of the patients had already been treated for AIHA and CLL was progressive regardless of AIHA in all patients but one. Overall response rates were 81% for AIHA and 77% for CLL. Median time to next treatment was 28.3 months and 26.2 months for AIHA and CLL, respectively. BR therapy may represent a good and safe therapeutic option in this setting where adequate control of CLL seems important for long-term AIHA response. Am. J. Hematol. 90:204–207, 2015.
- Published
- 2015
10. Wireless Video-Capsule Endoscopy Is a More Sensitive Investigative Method Than Gastro-Intestinal Endoscopy and Biopsies for the Diagnosis
- Author
-
Micol, Jean-Baptiste, Coiteux, Valerie, Pascal, Laurent, louis terriou, Willekens, Christophe, Jouet, Jean-Pierre, Maunoury, Vincent, and Yakoub-Agha, Ibrahim
11. Efficacy of 5-Azacitidine on IDH1/2 Acute Myeloid Leukemia/Myelodysplastic Syndromes and Correlation with 2-Hydroxyglutarate Production
- Author
-
Willekens, Christophe, Saada, Veronique, Broutin, Sophie, Delahousse, Julia, ALINE RENNEVILLE, Petrovanu, Cynthia, Marzac, Christophe, Micol, Jean-Baptiste, Solary, Eric, Pasquier, Florence, Lazarovici, Julien, Ribrag, Vincent, Preudhomme, Claude, Quivoron, Cyril, Penard-Lacronique, Virginie, Paci, Angelo, and Botton, Stephane
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.