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  1. Article ; Online: Clinical impact of cytomorphology in mast cell leukemia.

    Valent, Peter

    American journal of hematology

    2023  Volume 99, Issue 1, Page(s) 6–8

    MeSH term(s) Humans ; Leukemia, Mast-Cell ; Bone Marrow ; Mast Cells
    Language English
    Publishing date 2023-11-06
    Publishing country United States
    Document type Editorial
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.27146
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mepolizumab in Hypereosinophilic Syndromes: Proposed Therapeutic Algorithm.

    Valent, Peter

    The journal of allergy and clinical immunology. In practice

    2022  Volume 10, Issue 9, Page(s) 2375–2377

    MeSH term(s) Algorithms ; Antibodies, Monoclonal, Humanized/therapeutic use ; Humans ; Hypereosinophilic Syndrome/drug therapy
    Chemical Substances Antibodies, Monoclonal, Humanized ; mepolizumab (90Z2UF0E52)
    Language English
    Publishing date 2022-09-10
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2843237-X
    ISSN 2213-2201 ; 2213-2198
    ISSN (online) 2213-2201
    ISSN 2213-2198
    DOI 10.1016/j.jaip.2022.06.027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: KIT D816V and the cytokine storm in mastocytosis: production and role of interleukin-6.

    Valent, Peter

    Haematologica

    2019  Volume 105, Issue 1, Page(s) 5–6

    MeSH term(s) Humans ; Interleukin-6 ; Mast Cells ; Mastocytosis/genetics ; Mastocytosis, Systemic/genetics ; Oncogenes
    Chemical Substances Interleukin-6
    Language English
    Publishing date 2019-12-24
    Publishing country Italy
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2019.234864
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Reversible Elevation of Tryptase Over the Individual's Baseline: Why is It the Best Biomarker for Severe Systemic Mast Cell Activation and MCAS?

    Valent, Peter / Akin, Cem / Arock, Michel

    Current allergy and asthma reports

    2024  Volume 24, Issue 3, Page(s) 133–141

    Abstract: Purpose of review: Mast cell (MC) activation syndromes (MCAS) are conditions defined by recurrent episodes of severe systemic anaphylaxis or similar systemic events triggered by MC-derived mediators that can be measured in biological fluids. Since some ... ...

    Abstract Purpose of review: Mast cell (MC) activation syndromes (MCAS) are conditions defined by recurrent episodes of severe systemic anaphylaxis or similar systemic events triggered by MC-derived mediators that can be measured in biological fluids. Since some symptoms of MC activation may occur due to other, non-MC etiologies and lead to confusion over diagnosis, it is of crucial importance to document the involvement of MC and their products in the patients´ symptomatology.
    Recent findings: The most specific and generally accepted marker of severe systemic MC activation is an event-related, transient increase in the serum tryptase level over the individual baseline of the affected individual. However, baseline concentrations of serum tryptase vary among donors, depending on the genetic background, age, kidney function, and underlying disease. As a result, it is of critical importance to provide a flexible equation that defines the diagnostic increase in tryptase qualifying as MCAS criterion in all patients, all situations, and all ranges of baseline serum tryptase. In 2012, the consensus group proposed the 120% + 2 ng/ml formula, which covers the great majority of groups, including cases with low, normal, or elevated basal serum tryptase level. This formula has been validated in subsequent studies and has proven to be a robust and consistent diagnostic criterion of MCAS. The present article is discussing the impact of this formula and possible limitations as well as alternative markers and mediators that may be indicative of MCAS.
    MeSH term(s) Humans ; Mast Cells ; Mastocytosis/diagnosis ; Tryptases ; Anaphylaxis/diagnosis ; Biomarkers
    Chemical Substances Tryptases (EC 3.4.21.59) ; Biomarkers
    Language English
    Publishing date 2024-02-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2057370-4
    ISSN 1534-6315 ; 1529-7322
    ISSN (online) 1534-6315
    ISSN 1529-7322
    DOI 10.1007/s11882-024-01124-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Oligo-monocytic CMML and other pre-CMML states: Clinical impact, prognostication and management.

    Valent, Peter

    Best practice & research. Clinical haematology

    2019  Volume 33, Issue 2, Page(s) 101137

    Abstract: Chronic myelomonocytic leukemia (CMML) is defined by myelodysplasia, pathologic accumulation of monocytes and a substantial risk to transform to secondary acute myeloid leukemia (sAML). In recent years, minimal diagnostic criteria for classical CMML and ... ...

    Abstract Chronic myelomonocytic leukemia (CMML) is defined by myelodysplasia, pathologic accumulation of monocytes and a substantial risk to transform to secondary acute myeloid leukemia (sAML). In recent years, minimal diagnostic criteria for classical CMML and CMML-variants were proposed. Moreover, potential pre-stages of CMML and interface conditions have been postulated. Oligomonocytic CMML is a condition where the absolute peripheral blood monocyte count does not reach a diagnostic level but all other criteria for CMML are fulfilled. Among potential pre-stages of CMML, clonal and non-clonal conditions have been described, including idiopathic monocytosis (IMUS) and clonal monocytosis of unknown significance (CMUS). Patients with myelodysplastic syndromes (MDS), clonal cytopenia of unknown significance (CCUS), clonal hematopoiesis of indeterminate potential (CHIP) and idiopathic cytopenia of undetermined significance (ICUS) may also progress to CMML. The current article provides an overview of pre-CMML conditions and oligomonocytic CMML, with special reference to diagnostic criteria, differential diagnoses, clinical outcomes and management.
    MeSH term(s) Clonal Hematopoiesis ; Diagnosis, Differential ; Humans ; Leukemia, Myelomonocytic, Chronic/diagnosis ; Leukemia, Myelomonocytic, Chronic/genetics ; Leukemia, Myelomonocytic, Chronic/metabolism ; Leukemia, Myelomonocytic, Chronic/therapy ; Mutation ; Myelodysplastic Syndromes/diagnosis ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; Myelodysplastic Syndromes/therapy ; Prognosis
    Language English
    Publishing date 2019-12-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2048027-1
    ISSN 1532-1924 ; 1521-6926
    ISSN (online) 1532-1924
    ISSN 1521-6926
    DOI 10.1016/j.beha.2019.101137
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book: Targeted genes in haematology

    Valent, Peter

    the PI3-kinase-Akt-mTOR pathway of signalling in leukaemic cells

    (European journal of clinical investigation ; 34, Suppl. 2)

    2004  

    Author's details guest ed.: Peter Valent
    Series title European journal of clinical investigation ; 34, Suppl. 2
    Collection
    Keywords Hämatologie ; Leukämie ; Signalkette
    Subject Signalkaskade ; Blutkrebs
    Language English
    Size 52 S. : Ill.
    Publisher Blackwell
    Publishing place Oxford
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT014180375
    Database Catalogue ZB MED Medicine, Health

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  7. Article ; Online: ICUS, IDUS, CHIP and CCUS: Diagnostic Criteria, Separation from MDS and Clinical Implications.

    Valent, Peter

    Pathobiology : journal of immunopathology, molecular and cellular biology

    2018  Volume 86, Issue 1, Page(s) 30–38

    Abstract: Various myeloid neoplasms, including the myelodysplastic syndromes (MDS), bear a certain risk of progression to secondary acute myeloid leukemia (sAML). The evolution from low-risk to high-risk MDS and finally to sAML suggests that leukemogenesis is a ... ...

    Abstract Various myeloid neoplasms, including the myelodysplastic syndromes (MDS), bear a certain risk of progression to secondary acute myeloid leukemia (sAML). The evolution from low-risk to high-risk MDS and finally to sAML suggests that leukemogenesis is a multistep process. However, even before an overt neoplasm, such as an MDS, develops, "prediagnostic" clonal conditions may be identified. With the advent of large-scale genomic screens, such conditions may be detected quite frequently and early in apparently healthy individuals. Recent data suggest that these conditions increase with age and are indeed associated with an increased risk of the occurrence of MDS or another myeloid neoplasm. In other patients, unexplained cytopenia may be detected and may precede MDS. More recently, diagnostic criteria for potential pre-MDS conditions, including idiopathic cytopenia of uncertain significance and clonal hematopoiesis with indeterminate potential, have been proposed. The current article provides an overview of pre-MDS states and related criteria through which these conditions can be discriminated from each other and from MDS. In addition, the clinical implications and management of pre-MDS states are discussed.
    MeSH term(s) Bone Marrow/pathology ; Diagnosis, Differential ; Disease Progression ; Hematopoiesis ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/etiology ; Myelodysplastic Syndromes/complications ; Myelodysplastic Syndromes/diagnosis ; Myeloproliferative Disorders/complications ; Myeloproliferative Disorders/diagnosis
    Language English
    Publishing date 2018-06-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1022703-9
    ISSN 1423-0291 ; 1015-2008
    ISSN (online) 1423-0291
    ISSN 1015-2008
    DOI 10.1159/000489042
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Cancer - A devastating disease, but also an eye-opener and window into the deep mysteries of life and its origins.

    Grunt, Thomas W / Valent, Peter

    Progress in biophysics and molecular biology

    2022  Volume 175, Page(s) 131–139

    Abstract: Although cancer is still the second leading cause of death worldwide, basic research has largely elucidated the underlying mechanisms that lead us deep into the laws of animate and inanimate nature. This review aims to demonstrate that the cancer process ...

    Abstract Although cancer is still the second leading cause of death worldwide, basic research has largely elucidated the underlying mechanisms that lead us deep into the laws of animate and inanimate nature. This review aims to demonstrate that the cancer process profoundly affects and reprograms fundamental principles and concepts of cellular life by harnessing the natural mechanisms of biological evolution. It is shown that mutation and selection - the drivers of cancer formation and progression - are mandatory consequences of Boltzmann's version of the second law of thermodynamics, which stipulates that entropy (or disorder) according to probability never decreases, followed by Darwinian evolution by filtering for the suitable geno- and karyotypes. Cancer research has shown that malignant cells can develop gradually or abruptly depending on the prevailing stress conditions. Similar principles were then observed in the evolution of species, referred to as micro- and macroevolution. Cancer cells can be related to phylogenetically older forms of life, and malignant transformation can be viewed as reverse (atavistic) evolution, accompanied by typical rearrangement of system information and loss of 'social' behavior. It becomes obvious that in nature no distinction is made between normal biology and pathobiology. Instead, everything follows the rules of natural evolution. This illustrates the depth of the cancer problem and may explain the serious difficulties faced in trying to eradicate cancer.
    MeSH term(s) Humans ; Biological Evolution ; Thermodynamics ; Entropy ; Neoplasms ; Mutation
    Language English
    Publishing date 2022-10-02
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 209302-9
    ISSN 1873-1732 ; 0079-6107
    ISSN (online) 1873-1732
    ISSN 0079-6107
    DOI 10.1016/j.pbiomolbio.2022.09.009
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  9. Article ; Online: KIT Mutations and Other Genetic Defects in Mastocytosis: Implications for Disease Pathology and Targeted Therapies.

    Chantran, Yannick / Valent, Peter / Arock, Michel

    Immunology and allergy clinics of North America

    2023  Volume 43, Issue 4, Page(s) 651–664

    Abstract: A KIT activating mutation (usually KIT D816V) is detected in neoplastic cells in greater than 90% of indolent patients with systemic mastocytosis (SM). In more advanced variants of SM, additional genetic defects can be found in several myeloid malignancy- ...

    Abstract A KIT activating mutation (usually KIT D816V) is detected in neoplastic cells in greater than 90% of indolent patients with systemic mastocytosis (SM). In more advanced variants of SM, additional genetic defects can be found in several myeloid malignancy-related genes, which can be detected by applying next-generation sequencing. Currently, the techniques recommended to detect the KIT D816V mutation and quantify the mutational burden in peripheral blood, bone marrow, or other organs/tissues are allele specific-quantitative PCR or droplet digital PCR. These techniques are useful for diagnosis, prognostication, follow-up and monitoring of therapeutic efficacy of cytoreductive agents in patients with SM.
    MeSH term(s) Humans ; Proto-Oncogene Proteins c-kit/genetics ; Mastocytosis/diagnosis ; Mastocytosis/genetics ; Mastocytosis/therapy ; Mutation ; Mastocytosis, Systemic/diagnosis ; Mastocytosis, Systemic/drug therapy ; Mastocytosis, Systemic/genetics ; Bone Marrow ; Mast Cells
    Chemical Substances Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
    Language English
    Publishing date 2023-06-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 92606-1
    ISSN 1557-8607 ; 0889-8561
    ISSN (online) 1557-8607
    ISSN 0889-8561
    DOI 10.1016/j.iac.2023.04.008
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  10. Book ; Online: Mastozytose, systemische

    Reiter, Andreas / Jawhar, Mohamad / Balabanov, Stefan / Bubnoff, Nikolas von / Panse, Jens Peter / Sperr, Wolfgang Reinhard / Valent, Peter

    Leitlinie : Empfehlungen der Fachgesellschaft zur Diagnostik und Therapie hämatologischer und onkologischer Erkrankungen : ICD-10: D47.0 (ISM), C96.2 (SM-AHN), C96.2 (ASM), C94.3- (MCL)

    (Onkopedia Leitlinien)

    2020  

    Abstract: Die systemische Mastozytose (SM) ist durch eine pathologische und individuell variable Vermehrung neoplastischer Mastzellen im Knochenmark (KM), in der Haut und in viszeralen Organen gekennzeichnet, insbesondere in Leber, Milz, Darm und Lymphknoten. Die ... ...

    Institution Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie
    Österreichische Gesellschaft für Hämatologie & Medizinische Onkologie
    Schweizerische Gesellschaft für Medizinische Onkologie
    Schweizerische Gesellschaft für Hämatologie
    Author's details DGHO - Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie e.V., OeGHO - Österreichische Gesellschaft für Hämatologie & Medizinische Onkologie, SSMO/SSOM/SGMO - Schweizerische Gesellschaft für Medizinische Onkologie, SGH-SSH - Schweizerische Gesellschaft für Hämatologie/Société Suisse d'Hématologie ; Autoren: Andreas Reiter, Mohamad Jawhar, Stefan Balabanov, Nikolas von Bubnoff, Jens Panse, Wolfgang Reinhard Sperr, Peter Valent
    Series title Onkopedia Leitlinien
    Abstract Die systemische Mastozytose (SM) ist durch eine pathologische und individuell variable Vermehrung neoplastischer Mastzellen im Knochenmark (KM), in der Haut und in viszeralen Organen gekennzeichnet, insbesondere in Leber, Milz, Darm und Lymphknoten. Die wesentlichen diagnostischen Kriterien umfassen kompakte Infiltrate von zumeist spindelzelligen Mastzellen, eine bei 80-95% der Patienten nachweisbare KIT D816 Mutation (>95% KIT D816V) und eine erhöhte Serumtryptase (>20 µg/l). Die durch eine Mastzellinfiltration verursachte klinisch fassbare Organbeteiligung entspricht den sogenannten B- und C-Findings, welche das Ausmaß der Organvergrößerung (z.B. Leber, Milz, Lymphknoten) und -dysfunktion (z.B. Zytopenie, Hypalbuminämie, portale Hypertonie, Malabsorption) kennzeichnen. Die WHO-Klassifikation umfasst zwei wesentliche Subkategorien: die indolente SM (ISM) und die fortgeschrittene SM (engl.: advanced SM, AdvSM). Die ISM ist weniger organinvasiv und hat keinen bzw. geringen Einfluss auf das Überleben. Die AdvSM ist organinvasiv und umfasst 3 Varianten: die aggressive SM (ASM), die SM mit assoziierter hämatologischer Neoplasie (SMAHN) und die Mastzell-Leukämie (MCL). Die SM-AHN ist die häufigste Variante (60-80%) der AdvSM. Die Begleitneoplasie ist in >95% der Patienten myeloischen Ursprungs, z.B. ein myelodysplastisches Syndrom (MDS), eine myeloproliferative Neoplasie (MPN), eine myelodysplastische/myeloproliferative Neoplasie (MDS/MPN) oder, am häufigsten, eine chronische myelomonozytäre Leukämie (CMML). Das mediane Überleben der Patienten mit AdvSM beträgt für die ASM 4 Jahre, für die SM-AHN 2-3 Jahre und für die MCL 0,5 - 1,5 Jahre. [...]
    Subject code 610
    Language German
    Size 1 Online-Ressource (24 Seiten), Diagramme
    Edition Stand: März 2020
    Publisher DGHO - Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie e.V
    Publishing place Berlin
    Publishing country Germany
    Document type Book ; Online
    Note Open Access
    HBZ-ID HT020591941
    DOI 10.4126/FRL01-006423173
    Database Repository for Life Sciences

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