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2. Tamoxifen for the treatment of myeloproliferative neoplasms: A Phase II clinical trial and exploratory analysis

Author

Fang, Zijian, Corbizi Fattori, Giuditta, McKerrell, Thomas, Boucher, Rebecca H., Jackson, Aimee, Fletcher, Rachel S., Forte, Dorian, Martin, Jose-Ezequiel, Fox, Sonia, Roberts, James, Glover, Rachel, Harris, Erica, Bridges, Hannah R., Grassi, Luigi, Rodriguez-Meira, Alba, Mead, Adam J., Knapper, Steven, Ewing, Joanne, Butt, Nauman M., Jain, Manish, Francis, Sebastian, Clark, Fiona J., Coppell, Jason, McMullin, Mary F., Wadelin, Frances, Narayanan, Srinivasan, Milojkovic, Dragana, Drummond, Mark W., Sekhar, Mallika, ElDaly, Hesham, Hirst, Judy, Paramor, Maike, Baxter, E. Joanna, Godfrey, Anna L., Harrison, Claire N., and Méndez-Ferrer, Simón

Published
2023
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3. A cholinergic neuroskeletal interface promotes bone formation during postnatal growth and exercise

Author

Gadomski, Stephen, Fielding, Claire, García-García, Andrés, Korn, Claudia, Kapeni, Chrysa, Ashraf, Sadaf, Villadiego, Javier, Toro, Raquel del, Domingues, Olivia, Skepper, Jeremy N., Michel, Tatiana, Zimmer, Jacques, Sendtner, Regine, Dillon, Scott, Poole, Kenneth E.S., Holdsworth, Gill, Sendtner, Michael, Toledo-Aral, Juan J., De Bari, Cosimo, McCaskie, Andrew W., Robey, Pamela G., and Méndez-Ferrer, Simón

Published
2022
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6. Bone Marrow Mesenchymal Stem Cells Support Acute Myeloid Leukemia Bioenergetics and Enhance Antioxidant Defense and Escape from Chemotherapy

Author

Forte, Dorian, García-Fernández, María, Sánchez-Aguilera, Abel, Stavropoulou, Vaia, Fielding, Claire, Martín-Pérez, Daniel, López, Juan Antonio, Costa, Ana S.H., Tronci, Laura, Nikitopoulou, Efterpi, Barber, Michael, Gallipoli, Paolo, Marando, Ludovica, Fernández de Castillejo, Carlos López, Tzankov, Alexandar, Dietmann, Sabine, Cavo, Michele, Catani, Lucia, Curti, Antonio, Vázquez, Jesús, Frezza, Christian, Huntly, Brian J., Schwaller, Juerg, and Méndez-Ferrer, Simón

Published
2020
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8. Remodeling of Bone Marrow Hematopoietic Stem Cell Niches Promotes Myeloid Cell Expansion during Premature or Physiological Aging

Author

Ho, Ya-Hsuan, del Toro, Raquel, Rivera-Torres, José, Rak, Justyna, Korn, Claudia, García-García, Andrés, Macías, David, González-Gómez, Cristina, del Monte, Alberto, Wittner, Monika, Waller, Amie K., Foster, Holly R., López-Otín, Carlos, Johnson, Randall S., Nerlov, Claus, Ghevaert, Cedric, Vainchenker, William, Louache, Fawzia, Andrés, Vicente, and Méndez-Ferrer, Simón

Published
2019
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11. Daily Onset of Light and Darkness Differentially Controls Hematopoietic Stem Cell Differentiation and Maintenance

Author

Golan, Karin, Kumari, Anju, Kollet, Orit, Khatib-Massalha, Eman, Subramaniam, Mohana Devi, Ferreira, Zulma S., Avemaria, Francesca, Rzeszotek, Sylwia, García-García, Andrés, Xie, Stephanie, Flores-Figueroa, Eugenia, Gur-Cohen, Shiri, Itkin, Tomer, Ludin-Tal, Aya, Massalha, Hassan, Bernshtein, Biana, Ciechanowicz, Andrzej K., Brandis, Alexander, Mehlman, Tevie, Bhattacharya, Suditi, Bertagna, Mayla, Cheng, Hui, Petrovich-Kopitman, Ekaterina, Janus, Tomasz, Kaushansky, Nathali, Cheng, Tao, Sagi, Irit, Ratajczak, Mariusz Z., Méndez-Ferrer, Simón, Dick, John E., Markus, Regina P., and Lapidot, Tsvee

Published
2018
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16. A Novel Systems-Biology Algorithm for the Analysis of Coordinated Protein Responses Using Quantitative Proteomics

Author

García-Marqués, Fernando, Trevisan-Herraz, Marco, Martínez-Martínez, Sara, Camafeita, Emilio, Jorge, Inmaculada, Lopez, Juan Antonio, Méndez-Barbero, Nerea, Méndez-Ferrer, Simón, del Pozo, Miguel Angel, Ibáñez, Borja, Andrés, Vicente, Sánchez-Madrid, Francisco, Redondo, Juan Miguel, Bonzon-Kulichenko, Elena, and Vázquez, Jesús

Published
2016
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17. Different niches for stem cells carrying the same oncogenic driver affect pathogenesis and therapy response in myeloproliferative neoplasms

Author

Grockowiak, Elodie, Korn, Claudia, Rak, Justyna, Lysenko, Veronika; https://orcid.org/0000-0002-6886-5444, Hallou, Adrien; https://orcid.org/0000-0002-3162-7848, Panvini, Francesca M, Williams, Matthew, Fielding, Claire, Fang, Zijian, Khatib-Massalha, Eman, García-García, Andrés; https://orcid.org/0000-0002-8797-649X, Li, Juan, Khorshed, Reema A, González-Antón, Sara, Baxter, E Joanna, Kusumbe, Anjali, Wilkins, Bridget S, Green, Anna, Simons, Benjamin D; https://orcid.org/0000-0002-3875-7071, Harrison, Claire N, Green, Anthony R, Lo Celso, Cristina; https://orcid.org/0000-0002-1163-4207, Theocharides, Alexandre P A; https://orcid.org/0000-0002-1535-8692, Méndez-Ferrer, Simón; https://orcid.org/0000-0002-9805-9988, Grockowiak, Elodie, Korn, Claudia, Rak, Justyna, Lysenko, Veronika; https://orcid.org/0000-0002-6886-5444, Hallou, Adrien; https://orcid.org/0000-0002-3162-7848, Panvini, Francesca M, Williams, Matthew, Fielding, Claire, Fang, Zijian, Khatib-Massalha, Eman, García-García, Andrés; https://orcid.org/0000-0002-8797-649X, Li, Juan, Khorshed, Reema A, González-Antón, Sara, Baxter, E Joanna, Kusumbe, Anjali, Wilkins, Bridget S, Green, Anna, Simons, Benjamin D; https://orcid.org/0000-0002-3875-7071, Harrison, Claire N, Green, Anthony R, Lo Celso, Cristina; https://orcid.org/0000-0002-1163-4207, Theocharides, Alexandre P A; https://orcid.org/0000-0002-1535-8692, and Méndez-Ferrer, Simón; https://orcid.org/0000-0002-9805-9988

Abstract

Aging facilitates the expansion of hematopoietic stem cells (HSCs) carrying clonal hematopoiesis-related somatic mutations and the development of myeloid malignancies, such as myeloproliferative neoplasms (MPNs). While cooperating mutations can cause transformation, it is unclear whether distinct bone marrow (BM) HSC-niches can influence the growth and therapy response of HSCs carrying the same oncogenic driver. Here we found different BM niches for HSCs in MPN subtypes. JAK-STAT signaling differentially regulates CDC42-dependent HSC polarity, niche interaction and mutant cell expansion. Asymmetric HSC distribution causes differential BM niche remodeling: sinusoidal dilation in polycythemia vera and endosteal niche expansion in essential thrombocythemia. MPN development accelerates in a prematurely aged BM microenvironment, suggesting that the specialized niche can modulate mutant cell expansion. Finally, dissimilar HSC-niche interactions underpin variable clinical response to JAK inhibitor. Therefore, HSC-niche interactions influence the expansion rate and therapy response of cells carrying the same clonal hematopoiesis oncogenic driver.

Published
2023

21. Inhibiting stromal cell heparan sulfate synthesis improves stem cell mobilization and enables engraftment without cytotoxic conditioning

Author

Saez, Borja, Ferraro, Francesca, Yusuf, Rushdia Z., Cook, Colleen M., Yu, Vionnie W.C., Pardo-Saganta, Ana, Sykes, Stephen M., Palchaudhuri, Rahul, Schajnovitz, Amir, Lotinun, Sutada, Lymperi, Stefania, Mendez-Ferrer, Simon, Toro, Raquel del, Day, Robyn, Vasic, Radovan, Acharya, Sanket S., Baron, Roland, Lin, Charles P., Yamaguchi, Yu, Wagers, Amy J., and Scadden, David T.

Published
2014
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22. Notch2 controls non-autonomous Wnt-signalling in chronic lymphocytic leukaemia

Author

Mangolini, Maurizio, Götte, Frederik, Moore, Andrew, Ammon, Tim, Oelsner, Madlen, Lutzny-Geier, Gloria, Klein-Hitpass, Ludger, Williamson, James C., Lehner, Paul J., Dürig, Jan, Möllmann, Michael, Rásó-Barnett, Lívia, Hughes, Katherine, Santoro, Antonella, Méndez-Ferrer, Simón, Oostendorp, Robert A. J., Zimber-Strobl, Ursula, Peschel, Christian, Hodson, Daniel J., Schmidt-Supprian, Marc, and Ringshausen, Ingo

Published
2018
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25. Sepsis promotes splenic production of a protective platelet pool with high CD40 ligand expression.

Author

Valet, Colin, Valet, Colin, Magnen, Mélia, Qiu, Longhui, Cleary, Simon J, Wang, Kristin M, Ranucci, Serena, Grockowiak, Elodie, Boudra, Rafik, Conrad, Catharina, Seo, Yurim, Calabrese, Daniel R, Greenland, John R, Leavitt, Andrew D, Passegué, Emmanuelle, Méndez-Ferrer, Simón, Swirski, Filip K, Looney, Mark R, Valet, Colin, Valet, Colin, Magnen, Mélia, Qiu, Longhui, Cleary, Simon J, Wang, Kristin M, Ranucci, Serena, Grockowiak, Elodie, Boudra, Rafik, Conrad, Catharina, Seo, Yurim, Calabrese, Daniel R, Greenland, John R, Leavitt, Andrew D, Passegué, Emmanuelle, Méndez-Ferrer, Simón, Swirski, Filip K, and Looney, Mark R

Abstract

Platelets have a wide range of functions including critical roles in hemostasis, thrombosis, and immunity. We hypothesized that during acute inflammation, such as in life-threatening sepsis, there are fundamental changes in the sites of platelet production and phenotypes of resultant platelets. Here, we showed during sepsis that the spleen was a major site of megakaryopoiesis and platelet production. Sepsis provoked an adrenergic-dependent mobilization of megakaryocyte-erythrocyte progenitors (MEPs) from the bone marrow to the spleen, where IL-3 induced their differentiation into megakaryocytes (MKs). In the spleen, immune-skewed MKs produced a CD40 ligandhi platelet population with potent immunomodulatory functions. Transfusions of post-sepsis platelets enriched from splenic production enhanced immune responses and reduced overall mortality in sepsis-challenged animals. These findings identify a spleen-derived protective platelet population that may be broadly immunomodulatory in acute inflammatory states such as sepsis.

Published
2022

26. A cholinergic neuroskeletal interface promotes bone formation during postnatal growth and exercise.

Author

Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Gadomski, Stephen, Fielding, Claire, García García, Andrés, Korn, Claudia, Kapeni, Chrysa, Ashraf, Sadaf, Villadiego Luque, Francisco Javier, Toro Estévez, Raquel del, Toledo Aral, Juan José, Méndez Ferrer, Simón, Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Gadomski, Stephen, Fielding, Claire, García García, Andrés, Korn, Claudia, Kapeni, Chrysa, Ashraf, Sadaf, Villadiego Luque, Francisco Javier, Toro Estévez, Raquel del, Toledo Aral, Juan José, and Méndez Ferrer, Simón

Abstract

The autonomic nervous system is a master regulator of homeostatic processes and stress responses. Sym pathetic noradrenergic nerve fibers decrease bone mass, but the role of cholinergic signaling in bone has remained largely unknown. Here, we describe that early postnatally, a subset of sympathetic nerve fibers un dergoes an interleukin-6 (IL-6)-induced cholinergic switch upon contacting the bone. A neurotrophic depen dency mediated through GDNF-family receptor-a2 (GFRa2) and its ligand, neurturin (NRTN), is established between sympathetic cholinergic fibers and bone-embedded osteocytes, which require cholinergic innerva tion for their survival and connectivity. Bone-lining osteoprogenitors amplify and propagate cholinergic signals in the bone marrow (BM). Moderate exercise augments trabecular bone partly through an IL-6-depen dent expansion of sympathetic cholinergic nerve fibers. Consequently, loss of cholinergic skeletal innerva tion reduces osteocyte survival and function, causing osteopenia and impaired skeletal adaptation to mod erate exercise. These results uncover a cholinergic neuro-osteocyte interface that regulates skeletogenesis and skeletal turnover through bone-anabolic effects.

Published
2022

27. Supplemental Information. A cholinergic neuroskeletal interface promotes bone formation during postnatal growth and exercise

Author

Gadomski, Stephen, Fielding, Claire, García-García, Andrés, Korn, Claudia, Kapeni, Chrysa, Ashraf, Sadaf, Villadiego, Javier, Toro, Raquel del, Domingues, Olivia, Skepper, Jeremy N., Michel, Tatiana, Zimmer, Jacques, Sendtner, Regine, Dillon, Scott, Poole, Kenneth E. S., Holdsworth, Gill, Sendtner, Michael, Toledo-Aral, Juan José, De Bari, Cosimo, McCaskie, Andrew W., Robey, Pamela G., Méndez-Ferrer, Simón, Gadomski, Stephen, Fielding, Claire, García-García, Andrés, Korn, Claudia, Kapeni, Chrysa, Ashraf, Sadaf, Villadiego, Javier, Toro, Raquel del, Domingues, Olivia, Skepper, Jeremy N., Michel, Tatiana, Zimmer, Jacques, Sendtner, Regine, Dillon, Scott, Poole, Kenneth E. S., Holdsworth, Gill, Sendtner, Michael, Toledo-Aral, Juan José, De Bari, Cosimo, McCaskie, Andrew W., Robey, Pamela G., and Méndez-Ferrer, Simón

Published
2022

28. Megakaryocyte Diversity in Ontogeny, Functions and Cell-Cell Interactions

Author

Council for Higher Education (Israel), Weizmann Institute of Science, Wellcome Trust, MRC Cambridge Stem Cell Institute, National Health Service (UK), European Commission, Japan Agency for Medical Research and Development, Cancer Research UK, Khatib-Massalha, Eman, Méndez-Ferrer, Simón, Council for Higher Education (Israel), Weizmann Institute of Science, Wellcome Trust, MRC Cambridge Stem Cell Institute, National Health Service (UK), European Commission, Japan Agency for Medical Research and Development, Cancer Research UK, Khatib-Massalha, Eman, and Méndez-Ferrer, Simón

Abstract

Hematopoietic stem cells (HSCs) rely on local interactions in the bone marrow (BM) microenvironment with stromal cells and other hematopoietic cells that facilitate their survival and proliferation, and also regulate their functions. HSCs and multipotent progenitor cells differentiate into lineage-specific progenitors that generate all blood and immune cells. Megakaryocytes (Mks) are hematopoietic cells responsible for producing blood platelets, which are essential for normal hemostasis and blood coagulation. Although the most prominent function of Mks is platelet production (thrombopoiesis), other increasingly recognized functions include HSC maintenance and host immune response. However, whether and how these diverse programs are executed by different Mk subpopulations remains poorly understood. This Perspective summarizes our current understanding of diversity in ontogeny, functions and cell-cell interactions. Cumulative evidence suggests that BM microenvironment dysfunction, partly caused by mutated Mks, can induce or alter the progression of a variety of hematologic malignancies, including myeloproliferative neoplasms (MPNs) and other disorders associated with tissue scarring (fibrosis). Therefore, as an example of the heterogeneous functions of Mks in malignant hematopoiesis, we will discuss the role of Mks in the onset and progression of BM fibrosis. In this regard, abnormal interactions between of Mks and other immune cells might directly contribute to fibrotic diseases. Overall, further understanding of megakaryopoiesis and how Mks interact with HSCs and immune cells has potential clinical implications for stem cell transplantation and other therapies for hematologic malignancies, as well as for treatments to stimulate platelet production and prevent thrombocytopenia.

Published
2022

29. The EHA Research Roadmap:Hematopoietic Stem Cells and Allotransplantation

Author

Fibbe, Willem, Bernardi, Rosa, Charbord, Pierre, Krause, Daniela, Lo Celso, Cristina, Méndez-Ferrer, Simón, Mummery, Christine, Oostendorp, Robert, Raaijmakers, Marc, Socié, Gerard, Staal, Frank, Bacigalupo, Andrea, Fibbe, Willem, Bernardi, Rosa, Charbord, Pierre, Krause, Daniela, Lo Celso, Cristina, Méndez-Ferrer, Simón, Mummery, Christine, Oostendorp, Robert, Raaijmakers, Marc, Socié, Gerard, Staal, Frank, and Bacigalupo, Andrea

Published
2022

31. The EHA Research Roadmap: Hematopoietic Stem Cells and Allotransplantation

Author

Fibbe, Willem, primary, Bernardi, Rosa, additional, Charbord, Pierre, additional, Krause, Daniela, additional, Lo Celso, Cristina, additional, Méndez-Ferrer, Simón, additional, Mummery, Christine, additional, Oostendorp, Robert, additional, Raaijmakers, Marc, additional, Socié, Gerard, additional, Staal, Frank, additional, and Bacigalupo, Andrea, additional

Published
2022
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32. Sepsis promotes splenic production of a protective platelet pool with high CD40 ligand expression

Author

Valet, Colin, primary, Magnen, Mélia, additional, Qiu, Longhui, additional, Cleary, Simon J., additional, Wang, Kristin M., additional, Ranucci, Serena, additional, Grockowiak, Elodie, additional, Boudra, Rafik, additional, Conrad, Catharina, additional, Seo, Yurim, additional, Calabrese, Daniel R., additional, Greenland, John R., additional, Leavitt, Andrew D., additional, Passegué, Emmanuelle, additional, Méndez-Ferrer, Simón, additional, Swirski, Filip K., additional, and Looney, Mark R., additional

Published
2022
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34. The EHA Research Roadmap

Author

Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, De Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Celso, Cristina Lo, Martens, Joost H.A., Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan-Lluis Vives, Yvernogeau, Laurent, Schuringa, Jan Jacob, Celso, Cristina, Martens, Joost, Schuringa, Jan, Laboratoire de Biologie du Développement [IBPS] (LBD), Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Università degli Studi di Pavia = University of Pavia (UNIPV), IMIM-Hospital del Mar, Generalitat de Catalunya, Josep Carreras Leukaemia Research Institute (IJC), Instituto de Salud Carlos III [Madrid] (ISC), IRCCS San Raffaele Scientific Institute [Milan, Italie], The Francis Crick Institute [London], Immunologie humaine, physiopathologie & immunothérapie (HIPI (UMR_S_976 / U976)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut de Recherche Saint-Louis - Hématologie Immunologie Oncologie (Département de recherche de l’UFR de médecine, ex- Institut Universitaire Hématologie-IUH) (IRSL), Université Paris Cité (UPCité), Lymphopoïèse (Lymphopoïèse (UMR_1223 / U1223 / U-Pasteur_4)), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Erasmus University Medical Center [Rotterdam] (Erasmus MC), Leiden University Medical Center (LUMC), Universiteit Leiden, University of Edinburgh, Università degli studi di Verona = University of Verona (UNIVR), University of Cambridge [UK] (CAM), Haukeland University Hospital, University of Bergen (UiB), Barcelona Institute of Science and Technology (BIST), Universitat Pompeu Fabra [Barcelona] (UPF), Princess Máxima Center for Pediatric Oncology [Utrecht, Netherlands], Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), John Radcliffe Hospital [Oxford University Hospital], Cyprus Institute of Neurology and Genetics, Universitätsklinikum Essen [Universität Duisburg-Essen] (Uniklinik Essen), University of Manchester [Manchester], Goethe-Universität Frankfurt am Main, Georg-Speyer-Haus, Imperial College London, Radboud University [Nijmegen], NHSBT, Universitat de Barcelona (UB), Institució Catalana de Recerca i Estudis Avançats (ICREA), Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM), University of Copenhagen = Københavns Universitet (UCPH), Hubrecht Institute [Utrecht, Netherlands], University Medical Center [Utrecht]-Royal Netherlands Academy of Arts and Sciences (KNAW), University Medical Center [Utrecht], Institut Gustave Roussy (IGR), Dynamique moléculaire de la transformation hématopoïétique (Dynamo), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, University Medical Center Groningen [Groningen] (UMCG), Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Università degli Studi di Pavia, Laboratoire d'Innovation Thérapeutique (LIT), Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Université de Paris (UP), Laboratoire de Biologie du Développement [Paris] (LBD), Institut Pasteur [Paris], Hubrecht Institute for Developmental Biology and Stem Cell Research, Ghevaert, Cedric [0000-0002-9251-0934], Gottgens, Berthold [0000-0001-6302-5705], Apollo - University of Cambridge Repository, and Stem Cell Aging Leukemia and Lymphoma (SALL)

Subjects
Medizin, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Bioinformatics, 03 medical and health sciences, 0302 clinical medicine, SINGLE-CELL, REVEALS, Medicine, Diseases of the blood and blood-forming organs, Molecular Biology, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, DAMAGE, 0303 health sciences, VASCULAR NICHE, business.industry, ORIGIN, Normal hematopoiesis, Hematology, 3. Good health, ddc, MODEL, 030220 oncology & carcinogenesis, Perspective, RC633-647.5, business, COMMITMENT, STEM-CELLS
Abstract

International audience; In 2016, the European Hematology Association (EHA) published the EHA Roadmap for European Hematology Research1 aiming to highlight achievements in the diagnostics and treatment of blood disorders, and to better inform European policy makers and other stakeholders about the urgent clinical and scientific needs and priorities in the field of hematology. Each section was coordinated by 1–2 section editors who were leading international experts in the field. In the 5 years that have followed, advances in the field of hematology have been plentiful. As such, EHA is pleased to present an updated Research Roadmap, now including 11 sections, each of which will be published separately. The updated EHA Research Roadmap identifies the most urgent priorities in hematology research and clinical science, therefore supporting a more informed, focused, and ideally a more funded future for European hematology research. The 11 EHA Research Roadmap sections include Normal Hematopoiesis; Malignant Lymphoid Diseases; Malignant Myeloid Diseases; Anemias and Related Diseases; Platelet Disorders; Blood Coagulation and Hemostatic Disorders; Transfusion Medicine; Infections in Hematology; Hematopoietic Stem Cell Transplantation; CAR-T and Other Cell-based Immune Therapies; and Gene Therapy.

Published
2021
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37. Effects of Tamoxifen on the Mutant Allele Burden and Disease Course in Patients with Myeloproliferative Neoplasms - Results of the Tamarin Study

Author

Harrison, Claire, Baxter, Joanna, Boucher, Rebecca H., McKerrell, Thomas, Jackson, Aimee, Fletcher, Rachel S, Mead, Adam J., Knapper, Steve, Ewing, Joanne, Butt, Nauman M, Jain, Manish, Francis, Sebastian, Clark, Fiona J, Coppell, Jason, McMullin, Mary Frances, Wadelin, Frances, Narayanan, Srinivasan, Milojkovic, Dragana, Drummond, Mark W., Sekhar, Mallika, Paramor, Maike, Roberts, James, Glover, Rachel, Harris, Erica, Grassi, Luigi, Rodriguez-Meira, Alba, Carroll, Jason, Martín, José-Ezequiel, Corbizi Fattori, Giuditta, Fang, Zijian, Godfrey, Anna L, and Méndez-Ferrer, Simón

Published
2020
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40. Bone marrow mesenchymal stromal cells support translation in refractory acute myeloid leukemia

Author

Lisi-Vega, Livia E., Pievani, Alice, García-Fernández, María, Forte, Dorian, Williams, Tim L., Serafini, Marta, and Méndez-Ferrer, Simón

Abstract

In acute myeloid leukemia (AML), malignant cells surviving chemotherapy rely on high mRNA translation and their microenvironmental metabolic support to drive relapse. However, the role of translational reprogramming in the niche is unclear. Here, we found that relapsing AML cells increase translation in their bone marrow (BM) niches, where BM mesenchymal stromal cells (BMSCs) become a source of eIF4A-cap-dependent translation machinery that is transferred to AML cells via extracellular vesicles (EVs) to meet their translational demands. In two independent models of highly chemo-resistant AML driven by MLL-AF9 or FLT3-ITD (internal tandem duplication) and nucleophosmin (NPMc) mutations, protein synthesis levels increase in refractory AML dependent on nestin+ BMSCs. Inhibiting cap-dependent translation in BMSCs abolishes their chemoprotective ability, while EVs from BMSCs carrying eIF4A boost AML cell translation and survival. Consequently, eIF4A inhibition synergizes with conventional chemotherapy. Together, these results suggest that AML cells rely on BMSCs to maintain an oncogenic translational program required for relapse.

Published
2025
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41. The EHA Research Roadmap: Normal Hematopoiesis

Author

Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, de Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Celso, Cristina Lo, Martens, Joost H A, Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan-Lluis Vives, Yvernogeau, Laurent, Schuringa, Jan Jacob, Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, de Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Celso, Cristina Lo, Martens, Joost H A, Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan-Lluis Vives, Yvernogeau, Laurent, and Schuringa, Jan Jacob

Published
2021

42. Heterotopic ossification in mice overexpressing Bmp2 in Tie2+ lineages

Author

Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Ministero de Ciencia, Innovación y Universidades, Prados, Belén, Toro Estévez, Raquel del, MacGrogan, Donal, Gómez-Apiñániz, Paula, Papoutsi, Tania, Muñoz-Cánoves, Pura, Méndez-Ferrer, Simón, Pompa, José Luis de la, Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Ministero de Ciencia, Innovación y Universidades, Prados, Belén, Toro Estévez, Raquel del, MacGrogan, Donal, Gómez-Apiñániz, Paula, Papoutsi, Tania, Muñoz-Cánoves, Pura, Méndez-Ferrer, Simón, and Pompa, José Luis de la

Abstract

Bone morphogenetic protein (Bmp) signaling is critical for organismal development and homeostasis. To elucidate Bmp2 function in the vascular/hematopoietic lineages we generated a new transgenic mouse line in which ectopic Bmp2 expression is controlled by the Tie2 promoter. Tie2CRE/+;Bmp2tg/tg mice develop aortic valve dysfunction postnatally, accompanied by pre-calcific lesion formation in valve leaflets. Remarkably, Tie2CRE/+;Bmp2tg/tg mice develop extensive soft tissue bone formation typical of acquired forms of heterotopic ossification (HO) and genetic bone disorders, such as Fibrodysplasia Ossificans Progressiva (FOP). Ectopic ossification in Tie2CRE/+;Bmp2tg/tg transgenic animals is accompanied by increased bone marrow hematopoietic, fibroblast and osteoblast precursors and circulating pro inflammatory cells. Transplanting wild-type bone marrow hematopoietic stem cells into lethally irradiated Tie2CRE/+;Bmp2tg/tg mice significantly delays HO onset but does not prevent it. Moreover, transplanting Bmp2-transgenic bone marrow into wild-type recipients does not result in HO, but hematopoietic progenitors contribute to inflammation and ectopic bone marrow colonization rather than to endochondral ossification. Conversely, aberrant Bmp2 signaling activity is associated with fibroblast accumulation, skeletal muscle fiber damage, and expansion of a Tie2+ fibro-adipogenic precursor cell population, suggesting that ectopic bone derives from a skeletal muscle resident osteoprogenitor cell origin. Thus, Tie2CRE/+;Bmp2tg/tg mice recapitulate HO pathophysiology, and might represent a useful model to investigate therapies seeking to mitigate disorders associated with aberrant extra-skeletal bone formation.

Published
2021

43. The eha research roadmap:normal hematopoiesis

Author

Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, De Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Lo Celso, Cristina, Martens, Joost H.A., Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan Lluis Vives, Yvernogeau, Laurent, Schuringa, Jan Jacob, Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, De Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Lo Celso, Cristina, Martens, Joost H.A., Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan Lluis Vives, Yvernogeau, Laurent, and Schuringa, Jan Jacob

Abstract

In 2016, the European Hematology Association (EHA) published the EHA Roadmap for European Hematology Research1 aiming to highlight achievements in the diagnostics and treatment of blood disorders, and to better inform European policy makers and other stakeholders about the urgent clinical and scientific needs and priorities in the field of hematology. Each section was coordinated by 1–2 section editors who were leading international experts in the field. In the 5 years that have followed, advances in the field of hematology have been plentiful. As such, EHA is pleased to present an updated Research Roadmap, now including 11 sections, each of which will be published separately. The updated EHA Research Roadmap identifies the most urgent priorities in hematology research and clinical science, therefore supporting a more informed, focused, and ideally a more funded future for European hematology research. The 11 EHA Research Roadmap sections include Normal Hematopoiesis; Malignant Lymphoid Diseases; Malignant Myeloid Diseases; Anemias and Related Diseases; Platelet Disorders; Blood Coagulation and Hemostatic Disorders; Transfusion Medicine; Infections in Hematology; Hematopoietic Stem Cell Transplantation; CAR-T and Other Cell-based Immune Therapies; and Gene Therapy.

Published
2021

44. Heterotopic ossification in mice overexpressing Bmp2 in Tie2+ lineages

Author

Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Fundación Pro CNIC, Prados, Belén, Toro, Raquel del, MacGrogan, Donal, Gómez-Apiñániz, Paula, Papoutsi,, Tania, Muñoz-Cánoves, Pura, Méndez-Ferrer, Simón, Pompa, José Luis de la, Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Fundación Pro CNIC, Prados, Belén, Toro, Raquel del, MacGrogan, Donal, Gómez-Apiñániz, Paula, Papoutsi,, Tania, Muñoz-Cánoves, Pura, Méndez-Ferrer, Simón, and Pompa, José Luis de la

Abstract

Bone morphogenetic protein (Bmp) signaling is critical for organismal development and homeostasis. To elucidate Bmp2 function in the vascular/hematopoietic lineages we generated a new transgenic mouse line in which ectopic Bmp2 expression is controlled by the Tie2 promoter. Tie2CRE/+;Bmp2tg/tg mice develop aortic valve dysfunction postnatally, accompanied by pre-calcific lesion formation in valve leaflets. Remarkably, Tie2CRE/+;Bmp2tg/tg mice develop extensive soft tissue bone formation typical of acquired forms of heterotopic ossification (HO) and genetic bone disorders, such as Fibrodysplasia Ossificans Progressiva (FOP). Ectopic ossification in Tie2CRE/+;Bmp2tg/tg transgenic animals is accompanied by increased bone marrow hematopoietic, fibroblast and osteoblast precursors and circulating pro-inflammatory cells. Transplanting wild-type bone marrow hematopoietic stem cells into lethally irradiated Tie2CRE/+;Bmp2tg/tg mice significantly delays HO onset but does not prevent it. Moreover, transplanting Bmp2-transgenic bone marrow into wild-type recipients does not result in HO, but hematopoietic progenitors contribute to inflammation and ectopic bone marrow colonization rather than to endochondral ossification. Conversely, aberrant Bmp2 signaling activity is associated with fibroblast accumulation, skeletal muscle fiber damage, and expansion of a Tie2+ fibro-adipogenic precursor cell population, suggesting that ectopic bone derives from a skeletal muscle resident osteoprogenitor cell origin. Thus, Tie2CRE/+;Bmp2tg/tg mice recapitulate HO pathophysiology, and might represent a useful model to investigate therapies seeking to mitigate disorders associated with aberrant extra-skeletal bone formation.

Published
2021

45. The eha research roadmap: normal hematopoiesis

Author

CMM Groep Coffer, Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, De Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Lo Celso, Cristina, Martens, Joost H.A., Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan Lluis Vives, Yvernogeau, Laurent, Schuringa, Jan Jacob, CMM Groep Coffer, Jaffredo, Thierry, Balduini, Alessandra, Bigas, Anna, Bernardi, Rosa, Bonnet, Dominique, Canque, Bruno, Charbord, Pierre, Cumano, Anna, Delwel, Ruud, Durand, Charles, Fibbe, Willem, Forrester, Lesley, De Franceschi, Lucia, Ghevaert, Cedric, Gjertsen, Bjørn, Gottgens, Berthold, Graf, Thomas, Heidenreich, Olaf, Hermine, Olivier, Higgs, Douglas, Kleanthous, Marina, Klump, Hannes, Kouskoff, Valerie, Krause, Daniela, Lacaud, George, Lo Celso, Cristina, Martens, Joost H.A., Méndez-Ferrer, Simón, Menendez, Pablo, Oostendorp, Robert, Philipsen, Sjaak, Porse, Bo, Raaijmakers, Marc, Robin, Catherine, Stunnenberg, Henk, Theilgaard-Mönch, Kim, Touw, Ivo, Vainchenker, William, Corrons, Joan Lluis Vives, Yvernogeau, Laurent, and Schuringa, Jan Jacob

Published
2021

48. Molecular interactome between HSCs and their niches

Author

Méndez-Ferrer, Simón, Méndez-Ferrer, Simón [0000-0002-9805-9988], and Apollo - University of Cambridge Repository

Subjects
Ecological niche, 0303 health sciences, Immunology, Bone Marrow Cells, Cell Biology, Hematology, Computational biology, Biology, Biochemistry, Interactome, Stem cell niche, 03 medical and health sciences, 0302 clinical medicine, 030220 oncology & carcinogenesis, Stem Cell Niche, 030304 developmental biology
Abstract

Because hematopoietic stem cells (HSCs) were found to require a bone marrow (BM) habitat for long-term function, many studies have attempted to dissect key cellular and molecular interactions between HSCs and their BM microenvironments or HSC niches. In this issue of Blood, Mende et al provide a computational method to infer potential ligand-receptor interactions between murine hematopoietic stem and progenitor cells (HSPCs) and their niche-forming cells.

Published
2019
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