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201. Advanced systemic mastocytosis: from molecular and genetic progress to clinical practice

Author

Ustun, Celalettin, Arock, Michel, Kluin-Nelemans, Hanneke C., Reiter, Andreas, Sperr, Wolfgang R., George, Tracy, Horny, Hans-Peter, Hartmann, Karin, Sotlar, Karl, Damaj, Gandhi, Hermine, Olivier, Verstovsek, Srdan, Metcalfe, Dean D., Gotlib, Jason, Akin, Cem, Valent, Peter, Ustun, Celalettin, Arock, Michel, Kluin-Nelemans, Hanneke C., Reiter, Andreas, Sperr, Wolfgang R., George, Tracy, Horny, Hans-Peter, Hartmann, Karin, Sotlar, Karl, Damaj, Gandhi, Hermine, Olivier, Verstovsek, Srdan, Metcalfe, Dean D., Gotlib, Jason, Akin, Cem, and Valent, Peter

Abstract

Systemic mastocytosis is a heterogeneous disease characterized by the accumulation of neoplastic mast cells in the bone marrow and other organ organs/tissues. Mutations in KIT, most frequently KIT D816V, are detected in over 80% of all systemic mastocytosis patients. While most systemic mastocytosis patients suffer from an indolent disease variant, some present with more aggressive variants, collectively called advanced systemic mastocytosis, which include aggressive systemic mastocytosis, systemic mastocytosis with an associated hematologic, clonal non mast cell-lineage disease, and mast cell leukemia. Whereas patients with indolent systemic mastocytosis have a near normal life expectancy, patients with advanced systemic mastocytosis have a reduced life expectancy. Although cladribine and interferon-alpha are of benefit in a group of patients with advanced systemic mastocytosis, no curative therapy is available for these patients except possible allogeneic hematopoietic stem cell transplantation. Recent studies have also revealed additional somatic defects (apart from mutations in KIT) in a majority of patients with advanced systemic mastocytosis. These include TET2, SRSF2, ASXL1, RUNX1, JAK2, and/or RAS mutations, which may adversely impact prognosis and survival in particular systemic mastocytosis with an associated hematological neoplasm. In addition, several additional signaling molecules involved in the abnormal proliferation of mast cells in systemic mastocytosis have been identified. These advances have led to a better understanding of the biology of advanced systemic mastocytosis and to the development of new targeted treatment concepts. Herein, we review the biology and pathogenesis of advanced systemic mastocytosis, with a special focus on novel molecular findings as well as current and evolving therapeutic options.

Published
2016

202. Cutaneous manifestations in patients with mastocytosis: Consensus report of the European Competence Network on Mastocytosis; The American Academy of Allergy, Asthma & Immunology; And the European Academy of Allergology and Clinical Immunology

Author

Austrian Science Fund, European Academy of Allergy and Clinical Immunology, German Research Foundation, National Institute of Allergy and Infectious Diseases (US), Hartmann, Karin, Escribano, Luis, Grattan, Clive, Brockow, Knut, Carter, Melody C., Álvarez-Twose, Iván, Matito, Almudena, Broesby-Olsen, Sigurd, Siebenhaar, Frank, Lange, Magdalena, Niedoszytko, Marek, Castells, Mariana, Oude Elberink, Joanna N. G., Bonadonna, Patrizia, Zanotti, Roberta, Hornick, Jason L., Torrelo, Antonio, Grabbe, Jürgen, Rabenhorst, Anja, Nedoszytko, Boguslaw, Butterfield, Joseph H., Gotlib, Jason, Reiter, Andreas, Radia, Deepti, Hermine, Olivier, Sotlar, Karl, George, Tracy I., Kristensen, Thomas K., Kluin-Nelemans, Hanneke C., Yavuz, Selim, Hägglund, Hans, Sperr, Wolfgang R., Schwartz, Lawrence B., Triggiani, Massimo, Maurer, Marcus, Nilsson, Gunnar, Horny, Hans-Peter, Arock, Michel, Orfao, Alberto, Metcalfe, Dean D., Akin, Cem, Valent, Peter, Austrian Science Fund, European Academy of Allergy and Clinical Immunology, German Research Foundation, National Institute of Allergy and Infectious Diseases (US), Hartmann, Karin, Escribano, Luis, Grattan, Clive, Brockow, Knut, Carter, Melody C., Álvarez-Twose, Iván, Matito, Almudena, Broesby-Olsen, Sigurd, Siebenhaar, Frank, Lange, Magdalena, Niedoszytko, Marek, Castells, Mariana, Oude Elberink, Joanna N. G., Bonadonna, Patrizia, Zanotti, Roberta, Hornick, Jason L., Torrelo, Antonio, Grabbe, Jürgen, Rabenhorst, Anja, Nedoszytko, Boguslaw, Butterfield, Joseph H., Gotlib, Jason, Reiter, Andreas, Radia, Deepti, Hermine, Olivier, Sotlar, Karl, George, Tracy I., Kristensen, Thomas K., Kluin-Nelemans, Hanneke C., Yavuz, Selim, Hägglund, Hans, Sperr, Wolfgang R., Schwartz, Lawrence B., Triggiani, Massimo, Maurer, Marcus, Nilsson, Gunnar, Horny, Hans-Peter, Arock, Michel, Orfao, Alberto, Metcalfe, Dean D., Akin, Cem, and Valent, Peter

Abstract

Cutaneous lesions in patients with mastocytosis are highly heterogeneous and encompass localized and disseminated forms. Although a classification and criteria for cutaneous mastocytosis (CM) have been proposed, there remains a need to better define subforms of cutaneous manifestations in patients with mastocytosis. To address this unmet need, an international task force involving experts from different organizations (including the European Competence Network on Mastocytosis; the American Academy of Allergy, Asthma & Immunology; and the European Academy of Allergology and Clinical Immunology) met several times between 2010 and 2014 to discuss the classification and criteria for diagnosis of cutaneous manifestations in patients with mastocytosis. This article provides the major outcomes of these meetings and a proposal for a revised definition and criteria. In particular, we recommend that the typical maculopapular cutaneous lesions (urticaria pigmentosa) should be subdivided into 2 variants, namely a monomorphic variant with small maculopapular lesions, which is typically seen in adult patients, and a polymorphic variant with larger lesions of variable size and shape, which is typically seen in pediatric patients. Clinical observations suggest that the monomorphic variant, if it develops in children, often persists into adulthood, whereas the polymorphic variant may resolve around puberty. This delineation might have important prognostic implications, and its implementation in diagnostic algorithms and future mastocytosis classifications is recommended. Refinements are also suggested for the diagnostic criteria of CM, removal of telangiectasia macularis eruptiva perstans from the current classification of CM, and removal of the adjunct solitary from the term solitary mastocytoma.

Published
2016

204. Mast cell sarcoma: new cases and literature review

Author

Monnier, Jilliana, primary, Georgin-Lavialle, Sophie, additional, Canioni, Danielle, additional, Lhermitte, Ludovic, additional, Soussan, Michael, additional, Arock, Michel, additional, Bruneau, Julie, additional, Dubreuil, Patrice, additional, Bodemer, Christine, additional, Chandesris, Marie-Olivia, additional, Lortholary, Olivier, additional, Hermine, Olivier, additional, and Damaj, Gandhi, additional

Published
2016
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206. Cutaneous manifestations in patients with mastocytosis: Consensus report of the European Competence Network on Mastocytosis; the American Academy of Allergy, Asthma & Immunology; and the European Academy of Allergology and Clinical Immunology

Author

Hartmann, Karin, primary, Escribano, Luis, additional, Grattan, Clive, additional, Brockow, Knut, additional, Carter, Melody C., additional, Alvarez-Twose, Ivan, additional, Matito, Almudena, additional, Broesby-Olsen, Sigurd, additional, Siebenhaar, Frank, additional, Lange, Magdalena, additional, Niedoszytko, Marek, additional, Castells, Mariana, additional, Oude Elberink, Joanna N.G., additional, Bonadonna, Patrizia, additional, Zanotti, Roberta, additional, Hornick, Jason L., additional, Torrelo, Antonio, additional, Grabbe, Jürgen, additional, Rabenhorst, Anja, additional, Nedoszytko, Boguslaw, additional, Butterfield, Joseph H., additional, Gotlib, Jason, additional, Reiter, Andreas, additional, Radia, Deepti, additional, Hermine, Olivier, additional, Sotlar, Karl, additional, George, Tracy I., additional, Kristensen, Thomas K., additional, Kluin-Nelemans, Hanneke C., additional, Yavuz, Selim, additional, Hägglund, Hans, additional, Sperr, Wolfgang R., additional, Schwartz, Lawrence B., additional, Triggiani, Massimo, additional, Maurer, Marcus, additional, Nilsson, Gunnar, additional, Horny, Hans-Peter, additional, Arock, Michel, additional, Orfao, Alberto, additional, Metcalfe, Dean D., additional, Akin, Cem, additional, and Valent, Peter, additional

Published
2016
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207. Long-term treatment with imatinib results in profound mast cell deficiency in Ph plus chronic myeloid leukemia

Author

Cerny-Reiterer, Sabine, Rabenhorst, Anja, Stefanzl, Gabriele, Herndlhofer, Susanne, Hoermann, Gregor, Muellauer, Leonhard, Baumgartner, Sigrid, Beham-Schmid, Christine, Sperr, Wolfgang R., Mannhalter, Christine, Sill, Heinz, Linkesch, Werner, Arock, Michel, Hartmann, Karin, Valent, Peter, Cerny-Reiterer, Sabine, Rabenhorst, Anja, Stefanzl, Gabriele, Herndlhofer, Susanne, Hoermann, Gregor, Muellauer, Leonhard, Baumgartner, Sigrid, Beham-Schmid, Christine, Sperr, Wolfgang R., Mannhalter, Christine, Sill, Heinz, Linkesch, Werner, Arock, Michel, Hartmann, Karin, and Valent, Peter

Abstract

Although mast cells (MC) play an important role in allergic reactions, their physiologic role remains unknown. In mice, several models of MC-deficiency have been developed. However, no comparable human model is available. We examined the in vitro-and in vivo effects of the KIT-targeting drug imatinib on growth and development of human MC. Imatinib was found to inhibit stem cell factor (SCF)-induced differentiation of MC in long-term suspension cultures (IC50: 0.01 mu M). Correspondingly, long-term treatment of chronic myeloid leukemia (CML) patients with imatinib (400 mg/day) resulted in a marked decrease in MC. In patients with continuous complete molecular response during therapy, bone marrow MC decreased to less than 5% of pre-treatment values, and also serum tryptase concentrations decreased significantly (pre-treatment: 32.0 +/- 11.1 ng/ml; post-therapy: 3.4 +/- 1.8, p<0.01). Other myeloid lineages, known to develop independently of KIT, were not affected by imatinib-therapy. Imatinib also produced a substantial decrease in MC-development in mice. However, no clinical syndrome attributable to drug-induced MC-deficiency was recorded in our CML patients. Together, imatinib suppresses MC production in vitro and in vivo. However, drug-induced MC depletion is not accompanied by adverse clinical events, suggesting that MC are less relevant to homeostasis in healthy tissues than we assumed so far.

Published
2015

208. KIT mutation analysis in mast cell neoplasms: Recommendations of the European Competence Network on Mastocytosis

Author

National Institute of Allergy and Infectious Diseases (US), Austrian Science Fund, Fundación Ramón Areces, Instituto de Salud Carlos III, Ligue Nationale contre le Cancer (France), Ministerio de Economía y Competitividad (España), Arock, Michel, Escribano, Luis, García-Montero, Andrés, Orfao, Alberto, Valent, Peter, National Institute of Allergy and Infectious Diseases (US), Austrian Science Fund, Fundación Ramón Areces, Instituto de Salud Carlos III, Ligue Nationale contre le Cancer (France), Ministerio de Economía y Competitividad (España), Arock, Michel, Escribano, Luis, García-Montero, Andrés, Orfao, Alberto, and Valent, Peter

Abstract

Although acquired mutations in KIT are commonly detected in various categories of mastocytosis, the methodologies applied to detect and quantify the mutant type and allele burden in various cells and tissues are poorly defined. We here propose a consensus on methodologies used to detect KIT mutations in patients with mastocytosis at diagnosis and during follow-up with sufficient precision and sensitivity in daily practice. In addition, we provide recommendations for sampling and storage of diagnostic material as well as a robust diagnostic algorithm. Using highly sensitive assays, KIT D816V can be detected in peripheral blood leukocytes from most patients with systemic mastocytosis (SM) that is a major step forward in screening and SM diagnosis. In addition, the KIT D816V allele burden can be followed quantitatively during the natural course or during therapy. Our recommendations should greatly facilitate diagnostic and follow-up investigations in SM in daily practice as well as in clinical trials. In addition, the new tools and algorithms proposed should lead to a more effective screen, early diagnosis of SM and help to avoid unnecessary referrals.

Published
2015

210. The underestimated role of basophils in Ph+ chronic myeloid leukaemia.

Author

Valent, Peter, Horny, Hans‐Peter, and Arock, Michel

Subjects
BASOPHILS, CHRONIC myeloid leukemia, ONCOGENES, DISEASE progression, DRUG resistance, HISTAMINE
Abstract

Abstract: Chronic myeloid leukaemia (CML) is a hematopoietic neoplasm defined by the chromosome translocation t(9;22) and the related oncogene, BCR‐ABL1. In most patients, leukaemic cells can be kept under control using BCR‐ABL1‐targeting drugs. However, many patients relapse which remains a clinical challenge. In particular, patients with advanced (accelerated or blast phase) CML have a poor prognosis. So far, little is known about molecular and cellular interactions and features that contribute to disease progression and drug resistance in CML. One key prognostic factor at diagnosis is marked basophilia. However, although basophils are well‐known multifunctional effector cells, their impact in CML remains uncertain. In this article, we discuss the potential role of basophils as active contributors to disease evolution and progression in CML. In particular, basophils serve as a unique source of inflammatory, angiogenic and fibrogenic molecules, such as vascular endothelial growth factor or hepatocyte growth factor. In addition, basophils provide vasoactive substances, like histamine as well as the cytokine‐degrading enzyme dipeptidyl‐peptidase IV which may promote stem cell mobilization and the extramedullary spread of stem and progenitor cells. Finally, basophils may produce autocrine growth factors for myeloid cells. Understanding the role of basophils in CML evolution and progression may support the development of more effective treatment concepts. [ABSTRACT FROM AUTHOR]

Published
2018
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211. Identification of a leukemia-initiating stem cell in human mast cell leukemia

Author

Eisenwort, Gregor, Sadovnik, Irina, Schwaab, Juliana, Jawhar, Mohamad, Keller, Alexandra, Stefanzl, Gabriele, Berger, Daniela, Blatt, Katharina, Hoermann, Gregor, Bilban, Martin, Willmann, Michael, Winding, Christiana, Sperr, Wolfgang R., Arock, Michel, Rülicke, Thomas, Reiter, Andreas, and Valent, Peter

Abstract

Mast cell leukemia (MCL) is a highly fatal malignancy characterized by devastating expansion of immature mast cells in various organs. Although considered a stem cell disease, little is known about MCL-propagating neoplastic stem cells. We here describe that leukemic stem cells (LSCs) in MCL reside within a CD34+/CD38−fraction of the clone. Whereas highly purified CD34+/CD38─cells engrafted NSGhSCFmice with fully manifesting MCL, no MCL was produced by CD34+/CD38+progenitors or the bulk of KIT+/CD34−mast cells. CD34+/CD38–MCL cells invariably expressed CD13 and CD133, and often also IL-1RAP, but did not express CD25, CD26 or CLL-1. CD34+/CD38–MCL cells also displayed several surface targets, including CD33, which was homogenously expressed on MCL LSCs in all cases, and the D816V mutant form of KIT. Although CD34+/CD38−cells were resistant against single drugs, exposure to combinations of CD33-targeting and KIT-targeting drugs resulted in LSC-depletion and markedly reduced engraftment in NSGhSCFmice. Together, MCL LSCs are CD34+/CD38−cells that express distinct profiles of markers and target antigens. Characterization of MCL LSCs should facilitate their purification and should support the development of LSC-eradicating curative treatment approaches in this fatal type of leukemia.

Published
2019
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212. The Data Registry of the European Competence Network on Mastocytosis (ECNM): Set Up, Projects, and Perspectives

Author

Valent, Peter, Oude Elberink, Joanna N.G., Gorska, Aleksandra, Lange, Magdalena, Zanotti, Roberta, van Anrooij, Björn, Bonifacio, Massimiliano, Bonadonna, Patrizia, Gleixner, Karoline V., Hadzijusufovic, Emir, Perkins, Cecelia, Hartmann, Karin, Illerhaus, Anja, Merante, Serena, Elena, Chiara, Shoumariyeh, Khalid, von Bubnoff, Nikolas, Parente, Roberta, Triggiani, Massimo, Schwaab, Juliana, Jawhar, Mohamad, Caroppo, Francesca, Fortina, Anna Belloni, Brockow, Knut, Fuchs, David, Greul, Rosemarie, Yavuz, Akif Selim, Doubek, Michael, Mattsson, Mattias, Hagglund, Hans, Panse, Jens, Sabato, Vito, Aberer, Elisabeth, Al-Ali, Haifa Kathrin, Morren, Marie-Anne, Varkonyi, Judit, Zink, Alexander, Niedoszytko, Marek, Niederwieser, Dietger, Malcovati, Luca, Reiter, Andreas, Kennedy, Vanessa, Gotlib, Jason, Lortholary, Olivier, Hermine, Olivier, Arock, Michel, Kluin-Nelemans, Hanneke, and Sperr, Wolfgang R.

Abstract

Mastocytosis is a unique hematologic neoplasm with complex biology and pathology and a variable clinical course. The disease can essentially be divided into cutaneous mastocytosis (CM) and systemic mastocytosis (SM). In adults, SM is diagnosed in most cases and manifests as either indolent or advanced disease. Patients with advanced SM have an unfavorable prognosis with reduced survival. However, so far, little is known about the prevalence of various categories of SM and about prognostic factors. In an attempt to learn more about the behavior and evolution of various forms of CM and SM, the European Competence Network on Mastocytosis (ECNM) initiated a mastocytosis registry in 2012. In this article, the set up and start phase of this registry are described. Until 2018, more than 3000 patients from 12 countries and 25 centers have been enrolled. In a majority of all patients, robust follow-up data and relevant clinical end points are available. Using this data set, a series of registry projects have been launched, with the aim to validate previously identified diagnostic and prognostic variables and to identify new disease-related and patient-related parameters in various forms of mastocytosis. Moreover, the core data set of the registry will be useful to establish multiparametric scoring systems through which prognostication and individualized management of patients with mastocytosis should improve in the foreseeable future.

Published
2019
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216. Long-term treatment with imatinib results in profound mast cell deficiency in Ph+ chronic myeloid leukemia

Author

Cerny-Reiterer, Sabine, primary, Rabenhorst, Anja, additional, Stefanzl, Gabriele, additional, Herndlhofer, Susanne, additional, Hoermann, Gregor, additional, Müllauer, Leonhard, additional, Baumgartner, Sigrid, additional, Beham-Schmid, Christine, additional, Sperr, Wolfgang R., additional, Mannhalter, Christine, additional, Sill, Heinz, additional, Linkesch, Werner, additional, Arock, Michel, additional, Hartmann, Karin, additional, and Valent, Peter, additional

Published
2014
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218. MYB-GATA1 fusion promotes basophilic leukaemia: involvement of interleukin-33 and nerve growth factor receptors.

Author

Ducassou, Stéphane, Prouzet‐Mauléon, Valérie, Deau, Marie‐Céline, Brunet de la Grange, Philippe, Cardinaud, Bruno, Soueidan, Hayssam, Quelen, Cathy, Brousset, Pierre, Pasquet, Jean‐Max, Moreau‐Gaudry, François, Arock, Michel, Mahon, François‐Xavier, and Lippert, Eric

Abstract

Acute basophilic leukaemia ( ABL) is a rare subtype of acute myeloblastic leukaemia. We previously described a recurrent t(X;6)(p11;q23) translocation generating an MYB-GATA1 fusion gene in male infants with ABL. To better understand its role, the chimeric MYB-GATA1 transcription factor was expressed in CD34-positive haematopoietic progenitors, which were transplanted into immunodeficient mice. Cells expressing MYB-GATA1 showed increased expression of markers of immaturity ( CD34), of granulocytic lineage ( CD33 and CD117), and of basophilic differentiation ( CD203c and FcϵRI). UT-7 cells also showed basophilic differentiation after MYB-GATA1 transfection. A transcriptomic study identified nine genes deregulated by both MYB-GATA1 and basophilic differentiation. Induction of three of these genes ( CCL23, IL1RL1, and NTRK1) was confirmed in MYB-GATA1-expressing CD34-positive cells by reverse transcription quantitative polymerase chain reaction. Interleukin ( IL)-33 and nerve growth factor ( NGF), the ligands of IL-1 receptor-like 1 ( IL1RL1) and neurotrophic receptor tyrosine kinase 1 ( NTRK1), respectively, enhanced the basophilic differentiation of MYB-GATA1-expressing UT-7 cells, thus demonstrating the importance of this pathway in the basophilic differentiation of leukaemic cells and CD34-positive primary cells. Finally, gene reporter assays confirmed that MYB and MYB-GATA1 directly activated NTRK1 and IL1RL1 transcription, leading to basophilic skewing of the blasts. MYB-GATA1 is more efficient than MYB, because of better stability. Our results highlight the role of IL-33 and NGF receptors in the basophilic differentiation of normal and leukaemic cells. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2017
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219. Inhibition of HMC-1 mast cell proliferation by vitamin E: involvement of the protein kinase B pathway

Author

Kempná, Petra, Reiter, Elke, Arock, Michel, Azzi, Angelo, Zingg, Jean-Marc, Laboratoire de Biologie et de Pharmacologie Appliquée (LBPA), École normale supérieure - Cachan (ENS Cachan)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Mécanique Appliquée, Université des sciences et de la Technologie d'Oran Mohamed Boudiaf [Oran] (USTO MB), Unité de Recherche Matériaux et Energies Renouvelables (URMER), and Université Aboubekr Belkaid - University of Belkaïd Abou Bekr [Tlemcen]

Subjects
MESH: Signal Transduction, Time Factors, MESH: Piperazines, Tocopherols, Apoptosis, Piperazines, MESH: Dose-Response Relationship, Drug, Glycogen Synthase Kinase 3, Phosphatidylinositol 3-Kinases, MESH: Vitamin E, Vitamin E, Mast Cells, Enzyme Inhibitors, Phosphorylation, MESH: Tocopherols, MESH: Glycogen Synthase Kinase 3, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, MESH: Oxidative Stress, MESH: Mast Cells, U937 Cells, MESH: Enzyme Inhibitors, Benzamides, Imatinib Mesylate, MESH: Hydrogen Peroxide, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Mitogen-Activated Protein Kinase 3, MESH: ras Proteins, Signal Transduction, MESH: Mitogen-Activated Protein Kinase 1, MESH: Cell Line, Tumor, Blotting, Western, Protein Serine-Threonine Kinases, MESH: U937 Cells, Models, Biological, MESH: Protein-Serine-Threonine Kinases, Cell Line, Tumor, Proto-Oncogene Proteins, MESH: Cell Proliferation, Humans, MESH: Blotting, Western, Cell Proliferation, Glycogen Synthase Kinase 3 beta, MESH: Humans, Dose-Response Relationship, Drug, MESH: Phosphorylation, MESH: Proto-Oncogene Proteins c-akt, MESH: Apoptosis, Cell Membrane, MESH: Time Factors, MESH: Models, Biological, Hydrogen Peroxide, MESH: 1-Phosphatidylinositol 3-Kinase, MESH: Proto-Oncogene Proteins, Oxidative Stress, Pyrimidines, MESH: Pyrimidines, ras Proteins, Proto-Oncogene Proteins c-akt, MESH: Cell Membrane
Abstract

The effects of four natural tocopherols on the proliferation and signaling pathways were examined in the human mastocytoma cell line (HMC-1). The four tocopherols inhibited HMC-1 cell proliferation with different potency (delta > alpha = gamma > beta). Growth inhibition correlated with the reduction of PKB (protein kinase B) phosphorylation by the different tocopherols. The reduction of PKB phosphorylation led to a decrease of its activity, as judged from a parallel reduction of GSKalpha/beta phosphorylation. The translocation of PKB to the membrane, as a response to receptor stimulation by NGFbeta, is also prevented by treatment with tocopherols. In the presence of PKC or PP2A inhibitors, the reduction of PKB phosphorylation by tocopherols was still observed, thus excluding the direct involvement of these enzymes. Other pathways, such as the Ras-stimulated ERK1/2 (extracellular signal responsive kinase) pathway, were not affected by tocopherol treatment. The tocopherols did not significantly change oxidative stress in HMC-1 cells, suggesting that the observed effects are not the result of a general reduction of oxidative stress. Thus, the tocopherols interfere with PKB phosphorylation and reduce proliferation of HMC-1 cells, possibly by modulating either phosphatidylinositol 3-kinase, a kinase phosphorylating PKB (PDK1/2), or a phosphatase that dephosphorylates it. Inhibition of proliferation and PKB signaling in HMC-1 cells by vitamin E suggests a role in preventing diseases with mast cell involvement, such as allergies, atherosclerosis, and tumorigenesis.

Published
2004

220. Chronic mast cell leukemia (MCL) with KIT S476I: a rare entity defined by leukemic expansion of mature mast cells and absence of organ damage

Author

Valent, Peter, primary, Berger, Jörg, additional, Cerny-Reiterer, Sabine, additional, Peter, Barbara, additional, Eisenwort, Gregor, additional, Hoermann, Gregor, additional, Müllauer, Leonhard, additional, Mannhalter, Christine, additional, Steurer, Michael, additional, Bettelheim, Peter, additional, Horny, Hans-Peter, additional, and Arock, Michel, additional

Published
2014
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221. A new human mast cell line expressing a functional IgE receptor converts to tumorigenic growth by KIT D816V transfection

Author

Saleh, Rosine, primary, Wedeh, Ghaith, additional, Herrmann, Harald, additional, Bibi, Siham, additional, Cerny-Reiterer, Sabine, additional, Sadovnik, Irina, additional, Blatt, Katharina, additional, Hadzijusufovic, Emir, additional, Jeanningros, Sylvie, additional, Blanc, Catherine, additional, Legarff-Tavernier, Magali, additional, Chapiro, Elise, additional, Nguyen-Khac, Florence, additional, Subra, Frédéric, additional, Bonnemye, Patrick, additional, Dubreuil, Patrice, additional, Desplat, Vanessa, additional, Merle-Béral, Hélène, additional, Willmann, Michael, additional, Rülicke, Thomas, additional, Valent, Peter, additional, and Arock, Michel, additional

Published
2014
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222. Molecular Defects in Mastocytosis

Author

Bibi, Siham, primary, Langenfeld, Florent, additional, Jeanningros, Sylvie, additional, Brenet, Fabienne, additional, Soucie, Erinn, additional, Hermine, Olivier, additional, Damaj, Gandhi, additional, Dubreuil, Patrice, additional, and Arock, Michel, additional

Published
2014
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224. ASXL1 but Not TET2 Mutations Adversely Impact Overall Survival of Patients Suffering Systemic Mastocytosis with Associated Clonal Hematologic Non-Mast-Cell Diseases

Author

Damaj, Gandhi, primary, Joris, Magalie, additional, Chandesris, Olivia, additional, Hanssens, Katia, additional, Soucie, Erinn, additional, Canioni, Danielle, additional, Kolb, Brigitte, additional, Durieu, Isabelle, additional, Gyan, Emanuel, additional, Livideanu, Cristina, additional, Chèze, Stephane, additional, Diouf, Momar, additional, Garidi, Reda, additional, Georgin-Lavialle, Sophie, additional, Asnafi, Vahid, additional, Lhermitte, Ludovic, additional, Lavigne, Christian, additional, Launay, David, additional, Arock, Michel, additional, Lortholary, Olivier, additional, Dubreuil, Patrice, additional, and Hermine, Olivier, additional

Published
2014
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225. CD44 is a RAS/STAT5-regulated invasion receptor that triggers disease expansion in advanced mastocytosis

Author

Mueller, Niklas, Wicklein, Daniel, Eisenwort, Gregor, Jawhar, Mohamad, Berger, Daniela, Stefanzl, Gabriele, Greiner, Georg, Boehm, Alexandra, Kornauth, Christoph, Muellauer, Leonhard, Sehner, Susanne, Hoermann, Gregor, Sperr, Wolfgang R., Staber, Philipp B., Jaeger, Ulrich, Zuber, Johannes, Arock, Michel, Schumacher, Udo, Reiter, Andreas, and Valent, Peter

Abstract

The Hermes receptor CD44 is a multifunctional adhesion molecule that plays an essential role in the homing and invasion of neoplastic stem cells in various myeloid malignancies. Although mast cells (MCs) reportedly express CD44, little is known about the regulation and function of this receptor in neoplastic cells in systemic mastocytosis (SM). We found that clonal CD34+/CD38− stem cells, CD34+/CD38+ progenitor cells, and CD117++/CD34− MCs invariably express CD44 in patients with indolent SM (ISM), SM with an associated hematologic neoplasm, aggressive SM, and MC leukemia (MCL). In addition, all human MCL-like cell lines examined (HMC-1, ROSA, and MCPV-1) displayed cytoplasmic and cell-surface CD44. We also found that expression of CD44 in neoplastic MCs depends on RAS-MEK and STAT5 signaling and increases with the aggressiveness of SM. Correspondingly, higher levels of soluble CD44 were measured in the sera of patients with advanced SM compared with ISM or cutaneous mastocytosis and were found to correlate with overall and progression-free survival. To investigate the functional role of CD44, a xenotransplantation model was employed using severe combined immunodeficient (SCID) mice, HMC-1.2 cells, and a short hairpin RNA (shRNA) against CD44. In this model, the shRNA-mediated knockdown of CD44 resulted in reduced MC expansion and tumor formation and prolonged survival in SCID mice compared with HMC-1.2 cells transduced with control shRNA. Together, our data show that CD44 is a RAS-MEK/STAT5-driven MC invasion receptor that correlates with the aggressiveness of SM. Whether CD44 can serve as therapeutic target in advanced SM remains to be determined in forthcoming studies.

Published
2018
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226. Tyrosine Kinase Inhibition in Mastocytosis

Author

Bibi, Siham and Arock, Michel

Abstract

Mastocytosis is a group of rare disorders characterized by abnormal accumulation of mast cells in one or several organs. Mastocytosis can be seen at any age; but, in adults, the disease is usually systemic and chronic. Patients with indolent systemic mastocytosis (SM) are usually treated symptomatically, but cytoreductive treatments are needed in more advanced SM. In most patients with SM, an activating KITD816V mutation is found. Thus, patients with advanced SM benefit from treatment with KIT-targeting tyrosine kinase inhibitors. However, none of these drugs are curative; new targeted drugs or combinations are still needed to improve patients’ outcome.

Published
2018
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227. European Competence Network on Mastocytosis (ECNM) : 10-year jubilee, update, and future perspectives

Author

Valent, Peter, Arock, Michel, Bonadonna, Patrizia, Brockow, Knut, Broesby-Olsen, Sigurd, Escribano, Luis, Gleixner, Karoline V, Grattan, Clive, Hadzijusufovic, Emir, Hägglund, Hans, Hermine, Olivier, Horny, Hans-Peter, Kluin-Nelemans, Hanneke C, Maurer, Marcus, Niedoszytko, Marek, Nedoszytko, Boguslaw, Nilsson, Gunnar, Oude-Elberink, Hanneke N G, Orfao, Alberto, Radia, Deepti, Reiter, Andreas, Siebenhaar, Frank, Sotlar, Karl, Sperr, Wolfgang R, Triggiani, Massimo, VanDoormaal, Jaap J, Várkonyi, Judit, Yavuz, Selim, Hartmann, Karin, Valent, Peter, Arock, Michel, Bonadonna, Patrizia, Brockow, Knut, Broesby-Olsen, Sigurd, Escribano, Luis, Gleixner, Karoline V, Grattan, Clive, Hadzijusufovic, Emir, Hägglund, Hans, Hermine, Olivier, Horny, Hans-Peter, Kluin-Nelemans, Hanneke C, Maurer, Marcus, Niedoszytko, Marek, Nedoszytko, Boguslaw, Nilsson, Gunnar, Oude-Elberink, Hanneke N G, Orfao, Alberto, Radia, Deepti, Reiter, Andreas, Siebenhaar, Frank, Sotlar, Karl, Sperr, Wolfgang R, Triggiani, Massimo, VanDoormaal, Jaap J, Várkonyi, Judit, Yavuz, Selim, and Hartmann, Karin

Abstract

The European Competence Network on Mastocytosis (ECNM) was initiated in 2002 as a multidisciplinary and multinational cooperative approach to increase awareness and to improve diagnosis and therapy of mastocytosis. The network is composed of local centers, physicians, and scientists who have dedicated their work to patients with mastocytosis. A strategic goal of the ECNM is to provide the best available information about the disease to patients and physicians. During the past 10 years, the ECNM has expanded to various countries and contributed successfully to the development of markers, definitions, and standards in the field of mastocytosis. Members of the ECNM organized Annual Meetings in Europe and two Working Conferences on Mastocytosis in Vienna (in 2005 and 2010), and initiated and supported several preclinical and clinical trials. In all these activities, representatives of the ECNM cooperate closely with their US colleagues, with patient-organizations in Europe and in the USA, and with other scientific networks. The ECNM also launched a mastocytosis registry that has been activated in 2012. Using the central database of this registry, cooperative multicenter studies, which should include sufficient numbers of patients and robust evaluations, will be conducted. These studies will increase our knowledge about optimal management and therapy of patients with mastocytosis in the future.

Published
2012
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228. Pathogenesis and classification of eosinophil disorders: a review of recent developments in the field.

Author

Valent, P, Gleich, Gerald J, Reiter, Andreas, Roufosse, Florence, Weller, Peter F, Hellmann, A, Metzgeroth, Georgia, Leiferman, Kristin M, Arock, Michel, Sotlar, K, Butterfield, Joseph H, Cerny-Reiterer, S, Mayerhofer, M, Vandenberghe, Peter, Haferlach, T, Bochner, Bruce S, Gotlib, Jason, Horny, H, Simon, Hans-Uwe, Klion, Amy D, Valent, P, Gleich, Gerald J, Reiter, Andreas, Roufosse, Florence, Weller, Peter F, Hellmann, A, Metzgeroth, Georgia, Leiferman, Kristin M, Arock, Michel, Sotlar, K, Butterfield, Joseph H, Cerny-Reiterer, S, Mayerhofer, M, Vandenberghe, Peter, Haferlach, T, Bochner, Bruce S, Gotlib, Jason, Horny, H, Simon, Hans-Uwe, and Klion, Amy D

Abstract

info:eu-repo/semantics/published

Published
2012

229. ICON: Eosinophil Disorders.

Author

Valent, Peter, Klion, Amy, Rosenwasser, Lanny, Arock, Michel, Bochner, Bruce, Butterfield, Joe, Gotlib, Jason, Haferlach, T, Hellmann, A, Horny, H, Leiferman, Kristin, Metzgeroth, Georgia, Matsumoto, K, Reiter, Andreas, Roufosse, Florence, Rothenberg, Marc, Simon, Hans-Uwe, Sotlar, K, Vandenberghe, Peter, Weller, Peter, Gleich, Gerald, Valent, Peter, Klion, Amy, Rosenwasser, Lanny, Arock, Michel, Bochner, Bruce, Butterfield, Joe, Gotlib, Jason, Haferlach, T, Hellmann, A, Horny, H, Leiferman, Kristin, Metzgeroth, Georgia, Matsumoto, K, Reiter, Andreas, Roufosse, Florence, Rothenberg, Marc, Simon, Hans-Uwe, Sotlar, K, Vandenberghe, Peter, Weller, Peter, and Gleich, Gerald

Abstract

SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2012

230. Cancer stem cell definitions and terminology: The devil is in the details

Author

Valent, Peter, Bonnet, Dominique, De Maria Marchiano, Ruggero, Lapidot, Tsvee, Copland, Mhairi, Melo, Junia V., Chomienne, Christine, Ishikawa, Fumihiko, Schuringa, Jan Jacob, Stassi, Giorgio, Huntly, Brian, Herrmann, Harald, Soulier, Jean, Roesch, Alexander, Schuurhuis, Gerrit Jan, Wöhrer, Stefan, Arock, Michel, Zuber, Johanne, Cerny-Reiterer, Sabine, Johnsen, Hans E., Andreeff, Michael, Eaves, Connie, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Valent, Peter, Bonnet, Dominique, De Maria Marchiano, Ruggero, Lapidot, Tsvee, Copland, Mhairi, Melo, Junia V., Chomienne, Christine, Ishikawa, Fumihiko, Schuringa, Jan Jacob, Stassi, Giorgio, Huntly, Brian, Herrmann, Harald, Soulier, Jean, Roesch, Alexander, Schuurhuis, Gerrit Jan, Wöhrer, Stefan, Arock, Michel, Zuber, Johanne, Cerny-Reiterer, Sabine, Johnsen, Hans E., Andreeff, Michael, Eaves, Connie, and De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583)

Abstract

The cancer stem cell (CSC) concept has important therapeutic implications, but its investigation has been hampered both by a lack of consistency in the terms used for these cells and by how they are defined. Evidence of their heterogeneous origins, frequencies and their genomic, as well as their phenotypic and functional, properties has added to the confusion and has fuelled new ideas and controversies. Participants in The Year 2011 Working Conference on CSCs met to review these issues and to propose a conceptual and practical framework for CSC terminology. More precise reporting of the parameters that are used to identify CSCs and to attribute responses to them is also recommended as key to accelerating an understanding of their biology and developing more effective methods for their eradication in patients. © 2012 Macmillan Publishers Limited. All rights reserved.

Published
2012

232. Imatinib Inhibits SCF-Induced Development Of Human Mast Cells In Vitro and Induces Profound and Selective Mast Cell Deficiency In Patients With Ph+ CML

Author

Cerny-Reiterer, Sabine, primary, Rabenhorst, Anja, additional, Stefanzl, Gabriele, additional, Herndlhofer, Susanne, additional, Blatt, Katharina, additional, Hoermann, Gregor, additional, Muellauer, Leonhard, additional, Baumgartner, Sigrid, additional, Beham-Schmid, Christine, additional, Sperr, Wolfgang R, additional, Linkesch, Werner, additional, Mannhalter, Christine, additional, Arock, Michel, additional, Hartmann, Karin, additional, and Valent, Peter, additional

Published
2013
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233. Bromodomain-Containing Protein 4 (BRD4): A Novel Marker and Drug Target Expressed In Neoplastic Cells In Advanced Mast Cell Neoplasms

Author

Wedeh, Ghaith, primary, Hadzijusufovic, Emir, additional, Cerny-Reiterer, Sabine, additional, Herrmann, Harald, additional, Blatt, Katharina, additional, Eisenwort, Gregor, additional, Hoermann, Gregor, additional, Sperr, Wolfgang R, additional, Müllauer, Leonhard, additional, Vakoc, Christopher R., additional, Bradner, James E, additional, Horny, Hans-Peter, additional, Willmann, Michael, additional, Zuber, Johannes, additional, Arock, Michel, additional, and Valent, Peter, additional

Published
2013
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234. International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) & European Competence Network on Mastocytosis (ECNM) consensus response criteria in advanced systemic mastocytosis

Author

Gotlib, Jason, primary, Pardanani, Animesh, additional, Akin, Cem, additional, Reiter, Andreas, additional, George, Tracy, additional, Hermine, Olivier, additional, Kluin-Nelemans, Hanneke, additional, Hartmann, Karin, additional, Sperr, Wolfgang R., additional, Brockow, Knut, additional, Schwartz, Lawrence B., additional, Orfao, Alberto, additional, DeAngelo, Daniel J., additional, Arock, Michel, additional, Sotlar, Karl, additional, Horny, Hans-Peter, additional, Metcalfe, Dean D., additional, Escribano, Luis, additional, Verstovsek, Srdan, additional, Tefferi, Ayalew, additional, and Valent, Peter, additional

Published
2013
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235. Distinctive Serum miRNA Profile in Mouse Models of Striated Muscular Pathologies

Author

Vignier, Nicolas, primary, Amor, Fatima, additional, Fogel, Paul, additional, Duvallet, Angélique, additional, Poupiot, Jérôme, additional, Charrier, Sabine, additional, Arock, Michel, additional, Montus, Marie, additional, Nelson, Isabelle, additional, Richard, Isabelle, additional, Carrier, Lucie, additional, Servais, Laurent, additional, Voit, Thomas, additional, Bonne, Gisèle, additional, and Israeli, David, additional

Published
2013
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237. The increasing roles of epigenetics in breast cancer: Implications for pathogenicity, biomarkers, prevention and treatment.

Author

Basse, Clémence and Arock, Michel

Abstract

Nowadays, the mechanisms governing the occurrence of cancer are thought to be the consequence not only of genetic defects but also of epigenetic modifications. Therefore, epigenetic has become a very attractive and increasingly investigated field of research in order to find new ways of prevention and treatment of neoplasia, and this is particularly the case for breast cancer (BC). Thus, this review will first develop the main known epigenetic modifications that can occur in cancer and then expose the future role that control of epigenetic modifications might play in prevention, prognostication, follow-up and treatment of BC. Indeed, epigenetic biomarkers found in peripheral blood might become new tools to detect BC, to define its prognostic and to predict its outcome, whereas epi-drugs might have an increasing potential of development in the next future. However, if DNA methyltransferase inhibitors and histone desacetylase inhibitors have shown encouraging results in BC, their action remains nonspecific. Thus, additional clinical studies are needed to evaluate more precisely the effects of these molecules, even if they have provided encouraging results in cotreatment and combined therapies. This review will also deal with the potential of RNA interference (RNAi) as epi-drugs. Finally, we will focus on the potential prevention of BC through epigenetic based on diet and we will particularly develop the possible place of isothiocyanates from cruciferous vegetables or of Genistein from soybean in a dietary program that might potentially reduce the risk of BC in large populations. [ABSTRACT FROM AUTHOR]

Published
2015
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238. Antibody-Based and Cell Therapies for Advanced Mastocytosis: Established and Novel Concepts.

Author

Valent, Peter, Akin, Cem, Arock, Michel, Gleixner, Karoline V., Greinix, Hildegard, Hermine, Olivier, Horny, Hans-Peter, Ivanov, Daniel, Orfao, Alberto, Rabitsch, Werner, Reiter, Andreas, Schulenburg, Axel, Sotlar, Karl, Sperr, Wolfgang R., and Ustun, Celalettin

Subjects
*HEMATOPOIETIC stem cell transplantation, *CELLULAR therapy, *MAST cell disease, *HEMATOLOGIC malignancies, *MAST cells
Abstract

Advanced systemic mastocytosis (SM) is a heterogeneous group of myeloid neoplasms characterized by an uncontrolled expansion of mast cells (MC) in one or more internal organs, SM-induced tissue damage, and poor prognosis. Advanced SM can be categorized into aggressive SM (ASM), MC leukemia (MCL), and SM with an associated hematologic neoplasm (SM–AHN). In a vast majority of all patients, neoplastic cells display a KIT mutation, mostly D816V and rarely other KIT variants. Additional mutations in other target genes, such as SRSF2, ASXL1, or RUNX1, may also be identified, especially when an AHN is present. During the past 10 years, improved treatment approaches have led to a better quality of life and survival in patients with advanced SM. However, despite the availability of novel potent inhibitors of KIT D816V, not all patients enter remission and others relapse, often with a multi-mutated and sometimes KIT D816V-negative disease exhibiting multi-drug resistance. For these patients, (poly)chemotherapy, antibody-based therapies, and allogeneic hematopoietic stem cell transplantation may be viable treatment alternatives. In this article, we discuss treatment options for patients with drug-resistant advanced SM, including novel KIT-targeting drugs, antibody-based drugs, and stem cell-eradicating therapies. [ABSTRACT FROM AUTHOR]

Published
2023
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239. European Competence Network on Mastocytosis (ECNM): 10-year jubilee, update, and future perspectives

Author

Valent, Peter, primary, Arock, Michel, additional, Bonadonna, Patrizia, additional, Brockow, Knut, additional, Broesby-Olsen, Sigurd, additional, Escribano, Luis, additional, Gleixner, Karoline V., additional, Grattan, Clive, additional, Hadzijusufovic, Emir, additional, Hägglund, Hans, additional, Hermine, Olivier, additional, Horny, Hans-Peter, additional, Kluin-Nelemans, Hanneke C., additional, Maurer, Marcus, additional, Niedoszytko, Marek, additional, Nedoszytko, Boguslaw, additional, Nilsson, Gunnar, additional, Oude-Elberink, Hanneke N. G., additional, Orfao, Alberto, additional, Radia, Deepti, additional, Reiter, Andreas, additional, Siebenhaar, Frank, additional, Sotlar, Karl, additional, Sperr, Wolfgang R., additional, Triggiani, Massimo, additional, VanDoormaal, Jaap J., additional, Várkonyi, Judit, additional, Yavuz, Selim, additional, and Hartmann, Karin, additional

Published
2012
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240. Cancer stem cell definitions and terminology: the devil is in the details

Author

Valent, Peter, primary, Bonnet, Dominique, additional, De Maria, Ruggero, additional, Lapidot, Tsvee, additional, Copland, Mhairi, additional, Melo, Junia V., additional, Chomienne, Christine, additional, Ishikawa, Fumihiko, additional, Schuringa, Jan Jacob, additional, Stassi, Giorgio, additional, Huntly, Brian, additional, Herrmann, Harald, additional, Soulier, Jean, additional, Roesch, Alexander, additional, Schuurhuis, Gerrit Jan, additional, Wöhrer, Stefan, additional, Arock, Michel, additional, Zuber, Johannes, additional, Cerny-Reiterer, Sabine, additional, Johnsen, Hans E., additional, Andreeff, Michael, additional, and Eaves, Connie, additional

Published
2012
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241. ICON: Eosinophil Disorders

Author

Valent, Peter, primary, Klion, Amy D., additional, Rosenwasser, Lanny J., additional, Arock, Michel, additional, Bochner, Bruce S., additional, Butterfield, Joseph H., additional, Gotlib, Jason, additional, Haferlach, Torsten, additional, Hellmann, Andrzej, additional, Horny, Hans-Peter, additional, Leiferman, Kristin M., additional, Metzgeroth, Georgia, additional, Matsumoto, Kenji, additional, Reiter, Andreas, additional, Roufosse, Florence, additional, Rothenberg, Marc E., additional, Simon, Hans-Uwe, additional, Sotlar, Karl, additional, Vandenberghe, Peter, additional, Weller, Peter F, additional, and Gleich, Gerald J, additional

Published
2012
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242. Definitions, Criteria and Global Classification of Mast Cell Disorders with Special Reference to Mast Cell Activation Syndromes: A Consensus Proposal

Author

Valent, Peter, primary, Akin, Cem, additional, Arock, Michel, additional, Brockow, Knut, additional, Butterfield, Joseph H., additional, Carter, Melody C., additional, Castells, Mariana, additional, Escribano, Luis, additional, Hartmann, Karin, additional, Lieberman, Philip, additional, Nedoszytko, Boguslaw, additional, Orfao, Alberto, additional, Schwartz, Lawrence B., additional, Sotlar, Karl, additional, Sperr, Wolfgang R., additional, Triggiani, Massimo, additional, Valenta, Rudolf, additional, Horny, Hans-Peter, additional, and Metcalfe, Dean D., additional

Published
2011
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244. The classification of systemic mastocytosis should include mast cell leukemia (MCL) and systemic mastocytosis with a clonal hematologic non–mast cell lineage disease (SM-AHNMD)

Author

Valent, Peter, primary, Arock, Michel, additional, Akin, Cem, additional, Sperr, Wolfgang R., additional, Reiter, Andreas, additional, Sotlar, Karl, additional, Hartmann, Karin, additional, George, Tracy I., additional, Brockow, Knut, additional, Kluin-Nelemans, Hanneke C., additional, Gotlib, Jason, additional, Metcalfe, Dean D., additional, and Horny, Hans-Peter, additional

Published
2010
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245. Pediatric Mastocytosis Is a Clonal Disease Associated with D816V and Other Activating c-KIT Mutations

Author

Bodemer, Christine, primary, Hermine, Olivier, additional, Palmérini, Fabienne, additional, Yang, Ying, additional, Grandpeix-Guyodo, Catherine, additional, Leventhal, Phillip S., additional, Hadj-Rabia, Smail, additional, Nasca, Laurent, additional, Georgin-Lavialle, Sophie, additional, Cohen-Akenine, Annick, additional, Launay, Jean-Marie, additional, Barete, Stéphane, additional, Feger, Frédéric, additional, Arock, Michel, additional, Catteau, Benoît, additional, Sans, Beatrix, additional, Stalder, Jean François, additional, Skowron, Francois, additional, Thomas, Luc, additional, Lorette, Gérard, additional, Plantin, Patrice, additional, Bordigoni, Pierre, additional, Lortholary, Olivier, additional, Prost, Yves de, additional, Moussy, Alain, additional, Sobol, Hagay, additional, and Dubreuil, Patrice, additional

Published
2010
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246. Masitinib (AB1010), a Potent and Selective Tyrosine Kinase Inhibitor Targeting KIT

Author

Dubreuil, Patrice, primary, Letard, Sébastien, additional, Ciufolini, Marco, additional, Gros, Laurent, additional, Humbert, Martine, additional, Castéran, Nathalie, additional, Borge, Laurence, additional, Hajem, Bérengère, additional, Lermet, Anne, additional, Sippl, Wolfgang, additional, Voisset, Edwige, additional, Arock, Michel, additional, Auclair, Christian, additional, Leventhal, Phillip S., additional, Mansfield, Colin D., additional, Moussy, Alain, additional, and Hermine, Olivier, additional

Published
2009
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248. Characterization of three human sec14p-like proteins: α-Tocopherol transport activity and expression pattern in tissues

Author

Zingg, Jean-Marc, primary, Kempna, Petra, additional, Paris, Marcel, additional, Reiter, Elke, additional, Villacorta, Luis, additional, Cipollone, Rita, additional, Munteanu, Adelina, additional, De Pascale, Clara, additional, Menini, Stefano, additional, Cueff, Alexandra, additional, Arock, Michel, additional, Azzi, Angelo, additional, and Ricciarelli, Roberta, additional

Published
2008
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250. Case-Control Cohort Study of Patients' Perceptions of Disability in Mastocytosis

Author

Hermine, Olivier, primary, Lortholary, Olivier, additional, Leventhal, Phillip S., additional, Catteau, Adeline, additional, Soppelsa, Frédérique, additional, Baude, Cedric, additional, Cohen-Akenine, Annick, additional, Palmérini, Fabienne, additional, Hanssens, Katia, additional, Yang, Ying, additional, Sobol, Hagay, additional, Fraytag, Sylvie, additional, Ghez, David, additional, Suarez, Felipe, additional, Barete, Stéphane, additional, Casassus, Philippe, additional, Sans, Beatrice, additional, Arock, Michel, additional, Kinet, Jean Pierre, additional, Dubreuil, Patrice, additional, and Moussy, Alain, additional

Published
2008
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