Hans‐Peter Horny

Ludwig-Maximilians-Universität München

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Document Type

Co-Authors

Peter Valent

Medical University of Vienna

147

Karl Sotlar

Paracelsus Medical University

122

Wolfgang R. Sperr

Medical University of Vienna

Michel Arock

Pitié-Salpêtrière Hospital

Karin Hartmann

University of Basel

Andreas Reiter

Heidelberg University

Jason Gotlib

Stanford University

Cem Akin

University of Michigan–Ann Arbor

Juliana Schwaab

University Medical Centre Mannheim

Andreas Reiter

Heidelberg University

Cooperative Institutions

Universidad de Salamanca

153

Misgav Ladach

147

Medical University of Vienna

130

Heidelberg University

123

Harvard University

111

Ludwig-Maximilians-Universität München

102

University Hospital Heidelberg

Dana-Farber Cancer Institute

National Institutes of Health

LMU Klinikum

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Clinical and Laboratory Parameters of Mast Cell Activation as Basis for the Formulation of Diagnostic Criteria

International Archives of Allergy and Immunology (2011)

Peter Valent Hans‐Peter Horny Massimo Triggiani Michel Arock

Mast cell (MC) activation occurs in a number of different pathologic conditions. Acute activation is commonly seen in patients with allergic reactions, with consecutive massive release of vasoactive and proinflammatory mediator substances from MCs, leading to the clinical signs and symptoms of anaphylaxis. In these patients, serum tryptase concentrations usually increase subtantially above baseline levels. Chronic MC activation is more difficult to diagnose, especially when symptoms are mild or atypical, and no underlying disease is found. In these patients, serum tryptase levels usually are normal. In a smaller group of patients, tryptase levels are constantly elevated and may point to an occult form of mastocytosis. These patients have to be examined for MC monoclonality, other criteria of a primary MC disease, non-MC hematopoietic neoplasms, and reactive disorders producing chronic MC activation or MC accumulation. In most patients in whom MC activation is found, histamine-induced symptoms can be documented and usually respond to treatment with histamine receptor antagonists or MC stabilizers. If this is not the case, alternative explanations for symptoms and differential diagnoses have to be considered.

Tryptase

Proinflammatory cytokine

10.1159/000323763

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Citations (51)

IL-8 as mediator in the microenvironment-leukaemia network in acute myeloid leukaemia

Scientific Reports (2015)

Alexander Kuett Christina Rieger Deborah Perathoner Tobias Herold Michaela Wagner

Abstract The bone marrow microenvironment is physiologically hypoxic with areas being as low as 1% O 2 , e.g. the stem cell niche. Acute myeloid leukaemia (AML) blasts misuse these bone marrow niches for protection by the local microenvironment, but also might create their own microenvironment. Here we identify IL-8 as a hypoxia-regulated cytokine in both AML cell lines and primary AML samples that is induced within 48 hours of severe hypoxia (1% O 2 ). IL-8 lacked effects on AML cells but induced migration in mesenchymal stromal cells (MSC), an integral part of the bone marrow. Accordingly, MSC were significantly increased in AML bone marrow as compared to healthy bone marrow. Interestingly, mononuclear cells obtained from healthy bone marrow displayed both significantly lower endogenous and hypoxia-induced production of IL-8. IL-8 mRNA expression in AML blasts from 533 patients differed between genetic subgroups with significantly lower expression of IL-8 in acute promyelocytic leukaemia (APL), while in non APL-AML patients with FLT ITD had the highest IL-8 expression. In this subgroup, high IL-8 expression was also prognostically unfavourable. In conclusion, hypoxia as encountered in the bone marrow specifically increases IL-8 expression of AML, which in turn impacts niche formation. High IL-8 expression might be correlated with poor prognosis in certain AML subsets.

Hypoxia

10.1038/srep18411

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Citations (61)

Diagnostic value of histology and immunohistochemistry in myelodysplastic syndromes

Leukemia Research (2007)

Hans‐Peter Horny Karl Sotlar Peter Valent

Histology

CD31

Tryptase

10.1016/j.leukres.2007.05.010

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Citations (52)

Identification of Basogranulin (BB1) as a Novel Immunohistochemical Marker of Basophils in Normal Bone Marrow and Patients With Myeloproliferative Disorders

American Journal of Clinical Pathology (2005)

Hermine Agis Maria‐Theresa Krauth Alexandra Böhm Isabella Mosberger Leonhard Müllauer

In myeloproliferative disorders (MPDs), basophils typically increase in number in the bone marrow (BM) and blood. In chronic myeloid leukemia (CML), basophilia is a diagnostic and prognostic variable. However, no reliable approach for routine detection and enumeration of basophils in BM sections is available. We applied the antibasogranulin antibody BB1 on paraffin-embedded BM sections in 21 control samples (normal BM), 45 patients with CML, 9 with chronic idiopathic myelofibrosis, 11 with polycythemia vera, 19 with essential thrombocythemia, and 7 with indolent systemic mastocytosis. As assessed by immunostaining of serial BM sections, BB1+ cells coexpressed myeloperoxidase, histidine decarboxylase, and leukosialin but did not express B- or T-cell–restricted antigens. BB1+ BM cells were found to be highly elevated in patients with CML compared with normal BM or other MPDs, with maximum counts found in accelerated phase CML (median, 160 cells/mm2). In summary, BB1 (basogranulin) is a new immunohistochemical basophil marker that should allow quantification of basophils in CML at diagnosis and during therapy.

Basophilia

Myeloproliferative Disorders

10.1309/m9fq-mqgf-6616-7n2x

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Citations (0)

Kutanes T-Zell-Lymphom vom Typ der Mycosis fungoides im Bereich des Lides und des Tränenweges

Klinische Monatsblätter für Augenheilkunde (1997)

Hassane Aaliouet Jens Martin Rohrbach Thomas‐Michael Wohlrab Hans‐Peter Horny Karsten Sönnichsen

Patient A 62-year-old former miner with silicosis of the lungs but otherwise in good general condition presented with a solid nodule in the nasal left lid area for a duration of three months Because of a central ulceration the reference diagnosis was basalioma. The tumour infiltrated the nasal part of the upper and lower eyelid and the tear ducts so that these were unrinseable. Similar lesions have been present since two years in other skin regions.

Nodule (geology)

10.1055/s-2008-1035016

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Citations (3)

Refinements in response criteria in systemic mastocytosis: reply to a proposal

European Journal Of Haematology (2010)

Peter Valent Cem Akin Wolfgang R. Sperr Hans‐Peter Horny Dean D. Metcalfe

10.1111/j.1600-0609.2010.01462.x

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Citations (1)

mice with conditional expression of a constitutively active kit Mast cell hyperplasia, B-cell malignancy, and intestinal inflammation in

Karin Hartmann Axel Roers Hans‐Peter Horny Thomas Kamradt Ronald Naumann

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Citations (0)

Superior Efficacy of Midostaurin Over Cladribine in Advanced Systemic Mastocytosis: A Registry-Based Analysis

Journal of Clinical Oncology (2022)

Johannes Lübke Juliana Schwaab Nicole Naumann Hans‐Peter Horny Christel Weiß

PURPOSE On the basis of data from the German Registry on Disorders of Eosinophils and Mast Cells, we compared the efficacy of midostaurin and cladribine in patients with advanced systemic mastocytosis (AdvSM). PATIENTS AND METHODS Patients with AdvSM (n = 139) were treated with midostaurin only (n = 63, 45%), cladribine only (n = 23, 17%), or sequentially (midostaurin-cladribine, n = 30, 57%; cladribine-midostaurin, n = 23, 43%). Prognosis was assessed through the Mutation-Adjusted Risk Score (MARS). Besides the comparison of efficacy between midostaurin and cladribine on response (eg, organ dysfunction, bone marrow mast cell [MC] infiltration, and tryptase), overall survival (OS), and leukemia-free survival, we focused on the impact of treatment on involved non-MC lineages, for example, monocytes or eosinophils, and the KIT D816V expressed allele burden. RESULTS Midostaurin only was superior to cladribine only with effects from responses on MC and non-MC lineages conferring on a significantly improved OS (median 4.2 v 1.9 years, P = .033) and leukemia-free survival (2.7 v 1.3 years, P = .044) on the basis of a propensity score–weighted analysis of parameters included in MARS. Midostaurin compensated the inferior efficacy of cladribine in first- and second-line treatment. On midostaurin in any line, response of eosinophilia did not improve its baseline adverse prognostic impact, whereas response of monocytosis proved to be a positive on-treatment parameter. Multivariable analysis allowed to establish three risk categories (low/intermediate/high) through the combination of MARS and the reduction of the KIT D816V expressed allele burden of ≥ 25% at month 6 (median OS not reached v 3.0 years v 1.0 year; P < .001). CONCLUSION In this registry-based analysis, midostaurin revealed superior efficacy over cladribine in patients with AdvSM. In midostaurin-treated patients, the combination of baseline MARS and molecular response provided a compelling three-tier risk categorization (MARSv2.0) for OS.

Cladribine

Midostaurin

Univariate analysis

10.1200/jco.21.01849

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Citations (33)

Limited duration of complete remission on ruxolitinib in myeloid neoplasms with PCM1-JAK2 and BCR-JAK2 fusion genes

Annals of Hematology (2014)

Juliana Schwaab Marcin Knut Claudia Haferlach Georgia Metzgeroth Hans‐Peter Horny

Ruxolitinib

Myeloproliferative neoplasm

Hematology