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  • 1
    Language: English
    In: Expert Review of Hematology, 01 June 2010, Vol.3(3), pp.247-249
    Keywords: Biomarkers ; Biomarkers, Pharmacological ; Mastocytosis;
    ISSN: 1747-4086
    E-ISSN: 1747-4094
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  • 2
    In: The New England Journal of Medicine, 2015, Vol.373(2), pp.163-172
    Description: This article provides an overview of recent developments concerning the physiology and pathobiology of mast cells and discusses current diagnostic and therapeutic approaches to mast-cell disorders, with an emphasis on mastocytosis. Mast cells, which are present in most tissues, mature in situ from hematopoietic progenitors and acquire unique features of local effector cells. These features vary, depending on the tissue microenvironment. This article provides an overview of recent developments concerning the physiology and pathobiology of mast cells. We discuss current diagnostic and therapeutic approaches to mast-cell disorders, with an emphasis on mastocytosis. Physiology and Pathophysiology of Mast Cells Mast cells develop from hematopoietic progenitors in response to stem-cell factor (KIT ligand), which is the ligand of the CD117 transmembrane tyrosine kinase receptor, encoded by KIT. CD117 regulates the growth, migration, . . .
    Keywords: United States–Us ; Physiology ; Cells ; Vascular Endothelial Growth Factor ; Cytokines ; Mastocytosis ; Histamine ; Allergies ; Tumor Necrosis Factor-Tnf ; Ligands ; Mitochondrial DNA ; Mast Cells ; Tufts University;
    ISSN: 0028-4793
    E-ISSN: 1533-4406
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  • 3
    Language: English
    In: Blood, 01 February 2018, Vol.131(5), pp.505-514
    Description: Anemia is quite frequently diagnosed in older individuals and is a key indicator of various reactive and clonal conditions. Many underlying diseases, like myelodysplastic syndrome (MDS), develop preferentially in elderly individuals. The prevalence of anemia at older age is increasing, and this is mainly attributable to more frequently applied diagnostics and demographic changes in our societies. The etiology of anemia at older age is complex and ranges from bone marrow failure syndromes to chronic kidney disease, and from nutritional deficiencies to inflammatory processes including inflammaging in immunosenescence. In a smaller number of cases, no clear-cut etiology is identified. These patients are referred to as unexplained anemia or idiopathic cytopenia of unknown significance. In others, somatic mutations in leukocytes are found, but diagnostic criteria for MDS or other hematologic diseases are not fulfilled, a condition termed clonal cytopenia of undetermined significance. Management of anemias at older age depends on (1) the severity of the anemia, (2) underlying condition(s), and (3) patient-related factors, including comorbidities. Even a mild anemia may substantially affect physical and cognitive capacities and quality of life. An underestimated aspect is that because of age-related changes, organ function such as erythropoietin production in the kidney may become suboptimal. Management and treatment of anemia in older patients often require a multidisciplinary approach and detailed investigations of organ function. In this article, we review current concepts around anemias at older age, with special emphasis on etiologies, clinical implications, and innovative concepts in the management of these patients.
    Keywords: Age of Onset–Blood ; Aged–Diagnosis ; Aged, 80 and Over–Epidemiology ; Aging–Etiology ; Anemia–Therapy ; Humans–Diagnosis ; Late Onset Disorders–Epidemiology ; Late Onset Disorders–Etiology ; Late Onset Disorders–Therapy ; Abridged;
    ISSN: 00064971
    E-ISSN: 1528-0020
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  • 4
    Language: English
    In: Blood, 16 March 2017, Vol.129(11), pp.1420-1427
    Description: Over the past few years, substantial advances have been made in understanding the pathogenesis, evolution, and complexity of mast cell neoplasms. New diagnostic and prognostic parameters and novel therapeutic targets with demonstrable clinical impact have been identified. Several of these new markers, molecular targets, and therapeutic approaches have been validated and translated into clinical practice. At the same time, the classification of mastocytosis and related diagnostic criteria have been refined and updated by the consensus group and the World Health Organization (WHO). As a result, more specific therapies tailored toward prognostic subgroups of patients have been developed. Emerging treatment concepts use drugs directed against KIT and other relevant targets in neoplastic mast cells and will hopefully receive recognition by health authorities in the near future. This article provides an overview of recent developments in the field, with emphasis on the updated WHO classification, refined criteria, additional prognostic parameters, and novel therapeutic approaches. Based on these emerging concepts, the prognosis, quality of life, and survival of patients with advanced mastocytosis are expected to improve in the coming years.
    Keywords: Mastocytosis -- Classification
    ISSN: 00064971
    E-ISSN: 1528-0020
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  • 5
    In: PLoS ONE, 2013, Vol.8(7)
    Description: In chronic myelogenous (CML) and chronic eosinophilic leukemia (CEL), neoplastic cells spread via the circulation into various extramedullary organs. As E- and P-selectin constitute the starting point for the leucocyte adhesion/invasion cascade, and CEL and CML cells share many properties with normal granulocytes, we investigated the role of these selectins in CEL and CML cell expansion and organ invasion in a xenotransplantation model using scid mice. Using two human leukemic cell lines (EOL-1 and K562), we were able to show that E- and P-selectins mediate leukemia cell tethering and adherence in a laminar flow assay. While E-selectin binding depended on sialylated carbohydrate moieties, P-selectin binding was completely (K562) or partially (EOL-1) independent of these carbohydrates indicating the involvement of non-canonical selectin ligands. In a xenograft model in scid mice, both cell lines invaded the bone marrow and other organs, formed chloromas, and ultimately produced an overt leukemia. In contrast, in E- and P-selectin knockout scid mice, the cells failed to show engraftment in 8 out of 10 animals and even if they did engraft, they produced only little organ invasion and chloroma formation. Together, these data suggest that E- and P-selectins play an important role in leukemic dissemination in CML and CEL.
    Keywords: Research Article ; Biology ; Medicine
    E-ISSN: 1932-6203
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  • 6
    Language: English
    In: The Journal of Allergy and Clinical Immunology, December 2010, Vol.126(6), pp.1099-1104.e4
    Description: The term mast cell activation syndrome (MCAS) is finding increasing use as a diagnosis for subjects who present with signs and symptoms involving the dermis, gastrointestinal track, and cardiovascular system frequently accompanied by neurologic complaints. Such patients often have undergone multiple extensive medical evaluations by different physicians in varied disciplines without a definitive medical diagnosis until the diagnosis of MCAS is applied. However, MCAS as a distinct clinical entity has not been generally accepted, nor do there exist definitive criteria for diagnosis. Based on current understanding of this disease “syndrome” and on what we do know about mast cell activation and resulting pathology, we will explore and propose criteria for its diagnosis. The proposed criteria will be discussed in the context of other disorders involving mast cells or with similar presentations and as a basis for further scientific study and validation.
    Keywords: Mast Cells ; Tryptase ; Histamine ; Mastocytosis ; Allergy ; Anaphylaxis ; Urticaria ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 7
    Article
    Article
    Language: English
    In: The Journal of Allergy and Clinical Immunology, 2011, Vol.127(5), pp.1311-1312
    Description: [...]we take the position that the diagnosis of mastocytosis must continue to be based on the consensus criteria provided by the WHO4 rather than on symptoms alone, which could result in an inappropriate diagnosis, leading in turn to the application of an inappropriate and potentially harmful therapy.
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 8
    Language: English
    In: Current cancer drug targets, January 2011, Vol.11(1), pp.56-71
    Description: The concept of leukemic stem cells (LSC) is increasingly employed to explain the biology of various myeloid neoplasms and to screen for essential targets, with the hope to improve drug therapy through elimination of disease-initiating cells. Although the stem cell hypothesis may apply to all neoplasms, leukemia-initiating cells have so far only been characterized in some detail in advanced acute (AML) and chronic myeloid leukemia (CML). An intriguing observation is that although expressing various targets, LSC often remain unresponsive against most drugs, presumably because of 'intrinsic' resistance. Moreover, LSC represent heterogeneous populations of cells, grow in separate subclones, and acquire numerous defects, which points to substantial genetic instability and stem cell plasticity. The situation is complicated by the fact that stem cell evolution is a step-wise process with variable latency periods, so that many LSC-derived subclones remain small (undetectable) at diagnosis, but later, during therapy, may expand to a dominant clone and clinically overt relapsing disease. Finally the interaction between LSC and the microenvironment may contribute to stem cell function and LSC resistance. Taking all these considerations into account, the application of broadly acting targeted drugs and of drug combinations has been proposed in order to better suppress or even eliminate LSC in AML and CML. The current article provides a summary of our knowledge on LSC in various myeloid neoplasms with special reference to novel arising treatment concepts.
    Keywords: Leukemia, Myelogenous, Chronic, BCR-Abl Positive -- Drug Therapy ; Leukemia, Myeloid, Acute -- Drug Therapy ; Neoplastic Stem Cells -- Pathology
    ISSN: 15680096
    E-ISSN: 1873-5576
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  • 9
    Language: English
    In: Experimental Hematology, August 2013, Vol.41(8), pp.S5-S5
    Keywords: Medicine
    ISSN: 0301-472X
    E-ISSN: 1873-2399
    Source: ScienceDirect Journals (Elsevier)
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  • 10
    Language: English
    In: American journal of cancer research, 2013, Vol.3(2), pp.159-72
    Description: Mastocytosis is a rare disease characterized by abnormal expansion and accumulation of tissue mast cells (MC) in one or multiple organs. In most adult patients, systemic mastocytosis (SM) is diagnosed. Based on histopathological findings and organ damage, SM is divided into indolent SM (ISM), smoldering SM (SSM), SM with an associated hematologic non-MC-lineage disease (SM-AHNMD), aggressive SM (ASM), and MC leukemia (MCL). The clinical course and prognosis vary greatly among these groups of patients. In all variants of SM and most patients, neoplastic cells display the KIT mutation D816V. This suggests that additional KIT-independent molecular defects cause progression. Indeed, additional oncogenic lesions, including RAS- and TET2 mutations, have recently been identified in advanced SM. In patients with SM-AHNMD, such additional lesions are often detectable in the 'AHNMD-component' of the disease. Clinically relevant symptoms of SM result from i) malignant MC infiltration and the subsequent organ damage seen in advanced SM and/or ii) the release of pro-inflammatory and vasoactive mediators from MC, found in all disease-variants. Therapy of SM has to be adjusted to the individual situation in each patient. In ISM, the aim is to control mediator release and mediator effects. In advanced SM, a major goal is to control MC expansion by using conventional drugs or novel targeted drugs directed against mutant forms of KIT and/or other pro-oncogenic kinase-targets. In rapidly progressing ASM, MCL and drug-resistant AHNMD, chemotherapy and subsequent stem cell transplantation has to be considered.
    Keywords: Kit Mutations ; Mastocytosis ; Mast Cells ; Rare Disease ; Targeted Therapy
    ISSN: 2156-6976
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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