Peter Valent

Ludwig Boltzmann-Cluster Oncology (LB-CO) | Medical University Vienna, Wien, Vienna, Austria

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Publications (683)3249.02 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Mast cell leukemia (MCL) is a rare, life-threatening malignancy defined by a substantial increase in neoplastic mast cells (MCs) in bone marrow (BM) smears, drug-resistance, and a poor prognosis. In most patients, the survival time is less than 1 year. However, exceptional cases may present with a less malignant course. We report on a 49-year-old female patient with MCL diagnosed in 2013. In February 2013, first symptoms, including flushing, headache, and diarrhea, were recorded. In addition, mild anemia was detected. The disease was characterized by a massive increase in well-granulated, mature, and often spindle-shaped MCs (80 %) in BM smears. The serum tryptase level amounted to 332 ng/mL. Like in most other MCL patients, no skin lesions were detected. However, unlike in other patients, tryptase levels remained stable, and no other signs or symptoms of MCL-induced organ damage were found. Sequencing studies revealed an isolated S476I point mutation in KIT but no mutation in codon 816. The patient received histamine receptor blockers but refused cytoreductive therapy. After 9 months, still no progression or organ damage was detected. However, progression with transformation to acute MCL occurred after 12 months. We propose that the chronic type of MCL with stable conditions, absence of organ damage, and a mature MC morphology is recognized as a distinct entity that should be distinguished from the acute variant of MCL.
    Annals of Hematology 09/2014; · 2.87 Impact Factor
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    Peter Valent, Cem Akin, Michel Arock
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    ABSTRACT: Patients with systemic mastocytosis (SM) have an increased risk for the development of severe, life-threatening anaphylactic episodes. Despite prophylactic therapy with anti-mediator-type drugs, a mast cell (MC) activation syndrome (MCAS) may be diagnosed in these patients. In a subset of them, an immunoglobulin (Ig)E-dependent allergy is detected as underlying disease. The severity and frequency of anaphylactic reactions neither correlate with the burden of neoplastic MCs nor with specific IgE levels or the serum tryptase level. However, the ‘event-related’ increase in serum tryptase is usually indicative of a severe reaction. In addition, there is a positive correlation between severe anaphylaxis and the type of allergen in SM. In fact, many of these MCAS patients suffer from bee or wasp venom allergy. Currently recommended standard treatments for anaphylaxis in mastocytosis include the prophylactic use of histamine receptor (HR) antagonists, MC stabilizers, life-long immunotherapy in hymenoptera venom allergic patients, and epinephrine injections for emergency situations. In those who have an excessive burden of MCs (smouldering or aggressive SM) cladribine (2CdA) may be effective and may reduce the frequency of severe life-threatening events, and the same can sometimes be achieved with interferon-alpha (IFNα). In the future, additional treatment options, such as IgE-depletion or administration of tyrosine kinase inhibitors targeting IgE-dependent mediator secretion as well as KIT activation and thus MC expansion, may become standard therapy. Key points 1. Patients with mastocytosis have a high risk of developing severe anaphylaxis, especially when suffering from hymenoptera venom allergy, but sometimes also even in the absence of any known trigger or allergy. 2. Management of anaphylaxis in mastocytosis requires special considerations and special knowledge about potential triggers, disease pathogenesis, and treatment options and should be performed in, or in collaboration with, a specialized center.
    Current Treatment Options in Allergy. 09/2014; 1(3).
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    ABSTRACT: Aggressive systemic mastocytosis (ASM) is a rare but well-defined subtype of systemic mastocytosis (SM). The diagnosis of ASM is based on distinct morphological findings and the presence of clinical characteristics as consequence of SM-induced organ damage. Clinical findings of organ damage caused by massive mast cell infiltration are termed C-findings and include blood cytopenia, malabsorption with weight loss or signs of liver damage causing portal hypertension and ascites. Clinical features usually include hepatosplenomegaly and lymphadenopathy, the latter often presenting as retroperitoneal lymphadenopathy and thus initially mimicking malignant lymphoma. In most patients with C-findings, a bone marrow trephine biopsy is sufficient for a diagnosis of ASM to be established. Molecular testing in ASM almost always reveals the activating point mutation KIT D816V but also a variety of other point mutations, in particular in ASM cases associated with a non-mast cell hematological myeloid neoplasm. This disease combination is termed ASM with an associated hematological non-mast cell neoplasm (AHNMD) which is also the most frequent subtype of ASM, whereas ASM without an AHNMD (= “pure” ASM) only accounts for one-third of all ASM cases. The differential diagnoses of ASM and ASM-AHNMD include other subtypes of SM like mast cell leukemia and smoldering SM but also various myeloid neoplasms like myelomastocytic leukemia, chronic myelomonocytic leukemia, chronic eosinophilic leukemia, malignant histiocytosis, hairy cell leukemia, and even non-neoplastic inflammatory fibrotic conditions. Therefore, it is mandatory to apply a panel of mast cell-related antibodies on tissue sections including tryptase and CD117 expressed by mast cells at all stages of differentiation and maturation while aberrant expression of CD25 is exclusively seen in mastocytosis, especially in SM.
    The Journal of OncoPathology. 09/2014; 2(3).
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    ABSTRACT: During the past few years, a number of molecular markers have been developed in clinical hematology, most of them related to specific gene defects. However, there is also an unmet need to develop novel serologic parameters to improve diagnostics and prognostication in daily practice. Among these, the serum tryptase appears to be a most reliable biomarker of myeloid neoplasms. Elevated tryptase levels are found in subgroups of patients with mastocytosis, myelodysplastic syndrome, myeloproliferative neoplasm, acute myeloid leukemia, chronic myeloid leukemia and chronic eosinophilic leukemia. In these patients, the tryptase level is of diagnostic and/or prognostic significance. In mastocytosis, an elevated tryptase level is a minor criterion of systemic disease and in BCR-ABL1+ chronic myeloid leukemia, elevated tryptase at diagnosis correlates with treatment responses and overall survival. In patients with elevated tryptase, the enzyme also serves as follow-up parameter and can be employed to measure treatment-responses. In the current article, we review and update the perspectives of tryptase and provide recommendations for use of this conventional biomarker in daily practice.
    Expert Review of Hematology 08/2014; · 2.38 Impact Factor
  • Peter Valent
    Blood 08/2014; 124(9):1386-8. · 9.78 Impact Factor
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    ABSTRACT: Myelomastocytic leukemia (MML) is an extremely rare myeloid overlap-neoplasm that belongs to the group of tryptase-positive (T+) myeloid neoplasms. Main differential diagnoses include aggressive systemic mastocytosis (ASM), in particular ASM in transformation; mast cell leukemia; T+ acute myeloid leukemia (T+ AML); acute basophilic leukemia and chronic basophilic leukemia. MML exhibits both proliferative and dysplastic features and is characterized by prominent differentiation into the mast cell lineage in an advanced myeloid neoplasm, usually primary or secondary AML. While the histological key feature of MML is a diffuse increase in neoplastic cells expressing mast cell-related antigens like tryptase and CD117 (KIT), the most important cytomorphological finding in bone marrow (BM) and peripheral blood (PB) is the metachromatically granulated blast cell (= metachromatic blast). In contrast to systemic mastocytosis (SM), MML neither shows activating point mutations at codon 816 of KIT nor the aberrant expression of CD25 by mast cells is seen. MML can only be diagnosed when tryptase-staining is performed on BM biopsy specimens, PB and BM smears are investigated for presence of metachromatic blasts and other T+ leukemias have been excluded.
    Expert Review of Hematology 08/2014; 7(4):431-437. · 2.38 Impact Factor
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    ABSTRACT: House dust mites belong to the most potent indoor allergen sources worldwide and are associated with allergic manifestations in the respiratory tract and the skin. Here we studied the importance of the high molecular weight allergen, Der p 11, in HDM allergy. Sequence analysis showed that Der p 11 has high homology to paramyosins from mites, ticks and other invertebrates. A synthetic gene coding for Der p 11 was expressed in Escherichia coli and rDer p 11 purified to homogeneity as folded, alpha helical protein as determined by circular dichroism spectroscopy. Using antibodies raised against rDer p 11 and immunogold electron microscopy, the allergen was localized in the muscle beneath the skin of mite bodies but not in faeces. IgE reactivity of rDer p 11 was tested with sera from HDM allergic patients from Europe and Africa in RAST-based dot-blot assays. Interestingly, we found that Der p 11 is a major allergen for patients suffering from atopic dermatitis (AD), whereas it is only a minor allergen for patients suffering from respiratory forms of HDM allergy. Thus, rDer p 11 might be a useful serological marker allergen for the identification of a subgroup of HDM allergic patients suffering from HDM-associated AD.Journal of Investigative Dermatology accepted article preview online, 07 July 2014; doi:10.1038/jid.2014.271.
    The Journal of investigative dermatology. 07/2014;
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    ABSTRACT: Allogeneic haematopoietic stem cell transplantation (HSCT) is the only curative rescue-therapy for patients (pts) with chemotherapy-refractory acute leukaemia. Disease-control prior to HSCT is essential for long-term disease-free survival after HSCT.
    European Journal of Clinical Investigation 06/2014; · 3.37 Impact Factor
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    ABSTRACT: Definite progress has been made in the exploration of myelodysplastic syndromes by flow cytometry since the publication of the World Health Organization 2008 classification of myeloid neoplasms. An international working party initiated within the European LeukemiaNet and extended to include members from Australia, Canada, Japan, Taiwan and the United States has, through several workshops, developed and subsequently published consensus recommendations. The latter deal with preanalytical precautions, propose small and large panels, which allow evaluating immunophenotypic anomalies and calculating myelodysplasia scores. The current paper provides guidelines, which strongly recommend the integration of flow cytometry data with other diagnostic tools in diagnostic work-up of myelodysplastic syndromes.Leukemia accepted article preview online, 12 June 2014; doi:10.1038/leu.2014.191.
    Leukemia. 06/2014;
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    ABSTRACT: A total of 20 patients with cold antibody hemolytic anemia were evaluated in a retrospective study of them, 15 had a monoclonal gammopathy of unknown significance (MGUS): 14 with MGUS of immunoglobulin M (IgM) subtype and 1 with immunoglobulin G subtype. One patient had smoldering Waldenström's macroglobulinemia, but four patients had no monoclonal protein and no evidence of lymphoma. However, in three of these patients, we were able to demonstrate a (mono-)clonal rearrangement of their immunoglobulin heavy and/or light chains. Of the 20 patients, 5 had IgHV34 nucleotide sequence indicating that the antibody was directed against the "I" antigen. Two patients exhibited a progressive increase of IgM over time, however without increasing hemolytic activity. Moreover, in two patients with long-term follow-up, we were able to correlate recurrent hemolytic activity with low environmental temperatures. Among four patients treated with rituximab, all four responded to treatment. However, treatment effect was only transient in all of them.
    Wiener klinische Wochenschrift. 05/2014;
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    ABSTRACT: The CD52-targeted antibody alemtuzumab induces major clinical responses in a group of patients with myelodysplastic syndromes (MDS). The mechanism underlying this drug effect remains unknown. We asked whether neoplastic stem cells (NSC) in patients with MDS (n=29) or acute myeloid leukemia, AML (n=62) express CD52. As assessed by flow cytometry, CD52 was found to be expressed on NSC-enriched CD34+/CD38- cells in 8/11 patients with MDS and isolated del(5q). In most other MDS patients, CD52 was weakly expressed or not detectable on NSC. In AML, CD34+/CD38- cells displayed CD52 in 23/62 patients, including 4 with complex karyotype and del(5q) and one with del(5q) and t(1;17;X). In qPCR analyses, purified NSC obtained from del(5q) patients expressed CD52 mRNA. We were also able to show that CD52 mRNA levels correlate with EVI1 expression and that NRAS induces the expression of CD52 in AML cells. The CD52-targeting drug alemtuzumab was found to induce complement-dependent lysis of CD34+/CD38-/CD52+ NSC, but did not induce lysis in CD52- NSC. Alemtuzumab also suppressed engraftment of CD52+ NSC in NSG mice. Finally, CD52 expression on NSC was found to correlate with a poor survival in patients with MDS and AML. The cell surface target Campath-1 (CD52) is expressed on NSC in a group of patients with MDS and AML. CD52 is a novel prognostic NSC-marker and a potential NSC-target in a subset of patients with MDS and AML, which may have clinical implications and may explain clinical effects produced by alemtuzumab in these patients.
    Clinical Cancer Research 05/2014; · 7.84 Impact Factor
  • Hans-Peter Horny, Karl Sotlar, Peter Valent
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    ABSTRACT: Mastocytosis is a disease of bone marrow origin histologically characterized by compact tissue infiltrates of atypical mast cells never seen in reactive states. Most patients with mastocytosis have transformed mast cells carrying an activating point mutation at codon 816 of KIT and also show an elevated serum tryptase level. In this article immunophenotypical features of mast cells are described. Based on these features, mast cells are not closely related to other myeloid cells. Using the knowledge on aberrantly expressed antigens by mast cells, the hematopathologist should be able to recognize the disease even in the presence of unusual morphologic findings or an associated hematologic non-mast cell lineage disease.
    Immunology and allergy clinics of North America 05/2014; 34(2):315-321. · 3.18 Impact Factor
  • Cem Akin, Peter Valent
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    ABSTRACT: Mastocytosis is characterized by accumulation of pathologic mast cells in tissues. Most patients with mastocytosis experience mast cell activation symptoms in response to various triggers. The diagnosis of mastocytosis should be made from objective pathologic findings. Modern diagnostic criteria and classification of mastocytosis were proposed in 2000 by an international consensus group and formed the basis of the current World Health Organization (WHO) guidelines, which have been validated to correlate with prognosis and help selection of therapy. In this article, the WHO criteria for diagnosis and classification are summarized and practical aspects to avoid common pitfalls in diagnostic workup are discussed.
    Immunology and allergy clinics of North America 05/2014; 34(2):207-218. · 3.18 Impact Factor
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    ABSTRACT: Chronic myeloid leukemia (CML) is a stem cell (SC) neoplasm characterized by the BCR/ABL1 oncogene. Although mechanisms of BCR/ABL1-induced transformation are well-defined, little is known about effector-molecules contributing to malignant expansion and the extramedullary spread of leukemic SC (LSC) in CML. We have identified the cytokine-targeting surface enzyme dipeptidylpeptidase-IV (DPPIV=CD26) as a novel specific and pathogenetically relevant biomarker of CD34(+)/CD38(-) CML LSC. In functional assays, CD26 was identified as target-enzyme disrupting the SDF-1-CXCR4-axis by cleaving SDF-1, a chemotaxin recruiting CXCR4(+) SC. CD26 was not detected on normal SC or LSC in other hematopoietic malignancies. Correspondingly, CD26(+) LSC decreased to low or undetectable levels during successful treatment with imatinib. CD26(+) CML LSC engrafted NOD-SCID-IL-2Rγ(-/-) (NSG) mice with BCR/ABL1+ cells, whereas CD26(-) SC from the same patients produced multilineage BCR/ABL1-negative engraftment. Finally, targeting of CD26 by gliptins suppressed the expansion of BCR/ABL1+ cells. Together, CD26 is a new biomarker and target of CML LSC. CD26 expression may explain the abnormal extramedullary spread of CML LSC, and inhibition of CD26 may revert abnormal LSC function and support curative treatment approaches in this malignancy.
    Blood 04/2014; · 9.78 Impact Factor
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    ABSTRACT: Advanced systemic mastocytosis (SM) is an aggressive hematopoietic neoplasm with poor prognosis and short survival times. So far, no curative therapy is available for affected patients. We have identified the cell surface antigen CD52 (CAMPATH-1) as a molecular target expressed abundantly on the surface of primary neoplastic mast cells (MCs) in patients with advanced SM. In contrast, neoplastic MCs of patients with indolent SM and normal MCs expressed only low levels or did not express CD52. To study the mechanisms of CD52 expression and the value of this antigen as a potential therapeutic target, we generated a human MC cell line, designated MCPV-1, by lentiviral immortalization of cord blood-derived MC progenitor cells. Functional studies revealed that activated RAS profoundly promotes surface expression of CD52. The CD52-targeting antibody alemtuzumab induced cell death in CD52(+) primary neoplastic MCs obtained from patients with SM as well as in MCPV-1 cells. NSG mice xenotransplanted with MCPV-1 cells survived significantly longer after treatment with alemtuzumab (median survival: 31 d untreated vs. 46 d treated; P=0.0012). We conclude that CD52 is a novel marker and potential therapeutic target in neoplastic MCs in patients with advanced SM.-Hoermann, G., Blatt, K., Greiner, G. Putz, E. M., Berger, A., Herrmann, H., Cerny-Reiterer, S., Gleixner, K. V., Walz, C., Hoetzenecker, K., Müllauer, L., Reiter, A., Sotlar, K., Sexl, V., Valent, P., Mayerhofer, M. CD52 is a molecular target in advanced systemic mastocytosis.
    The FASEB Journal 04/2014; · 5.70 Impact Factor
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    ABSTRACT: Der p 23, a new, major house dust mite (HDM) allergen that is recognized by >70% of HDM-allergic patients, has high allergenic activity and, therefore, must be considered an important component for HDM-specific immunotherapy. We constructed and characterized a hypoallergenic Der p 23 vaccine for HDM immunotherapy. Three nonallergenic peptides from the C-terminal IgE epitope-containing part of Der p 23 (P4, P5) and P6, a mutant peptide containing serines instead of cysteines, were identified. Peptides were fused to the hepatitis B virus-derived PreS domain as recombinant fusion proteins (i.e., PreS-2XP4P5 and PreS-4XP6) that were expressed in Escherichia coli and purified to homogeneity. Compared with Der p 23, PreS-2XP4P5 and PreS-4XP6 showed no relevant IgE reactivity and exhibited considerably reduced allergenic activity in basophil activation tests using blood from HDM-allergic patients. Upon immunization of rabbits, only PreS-2XP4P5 induced high levels of Der p 23-specific IgG Abs that inhibited binding of patients' IgE to Der p 23, comparable to IgG Abs induced with Der p 23, whereas Abs induced with PreS-4XP6 had only low blocking capacity. Additionally, IgG Abs induced with PreS-2XP4P5 inhibited Der p 23-induced basophil activation comparable to IgG Abs induced with Der p 23. Compared with Der p 23, PreS-2XP4P5 induced lower T cell proliferation but higher levels of the tolerogenic cytokine IL-10 and the Th1 cytokine IFN-γ in PBMCs from HDM-allergic patients, indicating an immunomodulatory capacity of the fusion protein. Therefore, PreS-2XP4P5 represents a promising candidate for immunotherapy of HDM-allergic patients.
    The Journal of Immunology 04/2014; · 5.52 Impact Factor
  • Peter Valent
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    ABSTRACT: Several different risk factors and conditions may predispose to severe life-threatening anaphylaxis. Systemic mastocytosis (SM) is one such condition. Although many SM patients are suffering from mild or even no mediator-related symptoms, others have recurrent episodes of severe anaphylaxis, with clear signs of a mast cell activation syndrome (MCAS) despite prophylactic therapy with anti-mediator-type drugs. In several of these patients, an IgE-dependent allergy is diagnosed. The severity and frequency of MCAS-reactions neither correlate with the burden of neoplastic mast cells nor with the levels of specific IgE or the basal tryptase level. However, there is a relationship between severe anaphylaxis in SM and the type of allergen. Notably, many of these patients suffer from hymenoptera venom allergy. Currently recommended therapies include the prophylactic use of anti-mediator-type drugs, long-term immunotherapy for hymenoptera venom allergic patients, and epinephrine self-injector treatment for emergency-situations. In patients who present with an excess burden of mast cells, such as smouldering SM, cytoreductive therapy with cladribine (2CdA) may reduce the frequency of severe events. For the future, additional treatment options, such as IgE-depletion or the use of tyrosine kinase inhibitors blocking IgE-dependent mediator secretion as well as KIT activation may be useful alternatives.This article is protected by copyright. All rights reserved.
    Clinical & Experimental Allergy 04/2014; · 4.79 Impact Factor
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    ABSTRACT: KIT D816V is present in a majority of patients with systemic mastocytosis (SM). We determined the KIT D816V allele burden by quantitative real-time PCR in bone marrow and peripheral blood of 105 patients with mastocytosis. KIT D816V was detected in 92/105 patients (88%). Significant differences in the median allele burden were observed between disease subgroups: cutaneous mastocytosis (0.042%), indolent SM (0.285%), smoldering SM (5.991%), aggressive SM (9.346%), and SM with associated hematologic non-mast cell lineage disease (3.761%) (P < 0.001). The KIT D816V burden also correlated with serum tryptase (R = 0.5, P < 0.005) but not with mast cell infiltration in bone marrow or mediator symptoms. Moreover, the allele burden was of prognostic significance regarding survival (P < 0.01). Patients responding to cytoreductive therapy showed a significant decrease in KIT D816V (P < 0.05). To conclude, the KIT D816V burden correlates with the variant of mastocytosis, predicts survival, and is a valuable follow-up parameter in SM.
    Allergy 04/2014; · 5.88 Impact Factor
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    ABSTRACT: Mast cell leukemia (MCL), the leukemic manifestation of systemic mastocytosis (SM), is characterized by leukemic expansion of immature mast cells (MCs) in the bone marrow (BM) and other internal organs; and a poor prognosis. In a subset of patients, circulating MCs are detectable. A major differential diagnosis to MCL is myelomastocytic leukemia (MML). Although criteria for both MCL and MML have been published, several questions remain concerning terminologies and subvariants. To discuss open issues, the EU/US-consensus group and the European Competence Network on Mastocytosis (ECNM) launched a series of meetings and workshops in 2011-2013. Resulting discussions and outcomes are provided in this article. The group recommends that MML be recognized as a distinct condition defined by mastocytic differentiation in advanced myeloid neoplasms without evidence of SM. The group also proposes that MCL be divided into acute MCL and chronic MCL, based on the presence or absence of C-Findings. In addition, a primary (de novo) form of MCL should be separated from secondary MCL that typically develops in the presence of a known antecedent MC neoplasm, usually aggressive SM (ASM) or MC sarcoma. For MCL, an imminent prephase is also proposed. This prephase represents ASM with rapid progression and 5%-19% MCs in BM smears, which is generally accepted to be of prognostic significance. We recommend that this condition be termed ASM in transformation to MCL (ASM-t). The refined classification of MCL fits within and extends the current WHO classification; and should improve prognostication and patient selection in practice as well as in clinical trials.
    Annals of Oncology 03/2014; · 7.38 Impact Factor
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    ABSTRACT: In systemic mastocytosis (SM), clinical problems arise from factor-independent proliferation of mast cells (MCs) and the increased release of mediators by MCs. However, no human cell line model useful for studying MC activation in the context of SM is available. We have created a stable stem cell factor (SCF)-dependent human MC line, ROSA(KIT WT), expressing a fully functional IgE-receptor. Transfection with KIT D816V converted ROSA(KIT WT) cells into a SCF-independent clone, ROSA(KIT D816V) which produced a mastocytosis-like disease in NSG mice. However, although several signaling pathways are activated, ROSA(KIT D816V) did not exhibit an increased, but even a decreased responsiveness to IgE-dependent stimuli. Moreover, NSG mice bearing ROSA(KIT D816V)-derived tumors did not show mediator-related symptoms, and KIT D816V+ MCs obtained from patients with SM did not show increased IgE-dependent histamine release or CD63 up-regulation. In conclusion, our data show that KIT D816V is a disease-propagating oncoprotein but does not activate MCs to release proinflammatory mediators, which may explain why mediator-related symptoms in SM occur only in the context of a co-existing allergy. ROSA(KIT D816V) may provide a valuable tool for studying the pathogenesis of mastocytosis and should facilitate the development of novel drugs used to treat SM patients.
    Blood 03/2014; · 9.78 Impact Factor

Publication Stats

17k Citations
3,249.02 Total Impact Points

Institutions

  • 2008–2014
    • Ludwig Boltzmann-Cluster Oncology (LB-CO) | Medical University Vienna
      Wien, Vienna, Austria
    • Medizinische Universität Innsbruck
      • Univ.-Klinik für Innere Medizin V (Hämatologie und Onkologie)
      Innsbruck, Tyrol, Austria
  • 2007–2014
    • Hanusch Krankenhaus
      Wien, Vienna, Austria
    • Kumamoto University
      • Graduate School of Medical Sciences
      Kumamoto-shi, Kumamoto Prefecture, Japan
  • 1989–2014
    • Medical University of Vienna
      • • Institute for Social Medicine
      • • Klinische Abteilung für Onkologie
      • • Zentrum für Pathophysiologie, Infektiologie und Immunologie
      Wien, Vienna, Austria
  • 2013
    • CeMM Research Center for Molecular Medicine
      Wien, Vienna, Austria
    • Stanford Medicine
      Stanford, California, United States
  • 1999–2013
    • Vienna General Hospital
      Wien, Vienna, Austria
    • European Molecular Biology Laboratory
      Heidelburg, Baden-Württemberg, Germany
    • ORTON Foundation, Helsinki, Finland
      Helsinki, Southern Finland Province, Finland
  • 1995–2013
    • IST Austria
      Klosterneuberg, Lower Austria, Austria
    • Institute of Molecular Biology
      Mayence, Rheinland-Pfalz, Germany
  • 2012
    • University of Cologne
      • Department of Dermatology and Venerology
      Köln, North Rhine-Westphalia, Germany
  • 2010–2012
    • Ludwig-Maximilian-University of Munich
      • Institute of Pathology
      München, Bavaria, Germany
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
    • University Medical Center Schleswig-Holstein
      Kiel, Schleswig-Holstein, Germany
  • 2007–2012
    • Austrian Academy of Sciences
      • Forschungszentrum für Molekulare Medizin (CeMM)
      Vienna, Vienna, Austria
    • University of Veterinary Medicine in Vienna
      • Department for Companion Animals and Horses
      Vienna, Vienna, Austria
  • 2011
    • Evangelische Hochschule Freiburg, Germany
      Freiburg, Baden-Württemberg, Germany
  • 2010–2011
    • University of Michigan
      • Department of Internal Medicine
      Ann Arbor, MI, United States
  • 2009
    • Medical University of Gdansk
      Danzig, Pomeranian Voivodeship, Poland
  • 1988–2009
    • University of Vienna
      • • Universitätsklinik für Innere Medizin I
      • • Institute of Histology and Embryology
      • • Institute of Social Medicine
      Wien, Vienna, Austria
  • 1997–2008
    • University of Tuebingen
      • Institute of Pathology and Neuropathology
      Tübingen, Baden-Wuerttemberg, Germany
  • 2006
    • Universitätsklinikum Schleswig - Holstein
      • Institut für Pathologie (Kiel)
      Kiel, Schleswig-Holstein, Germany
    • Mayo Foundation for Medical Education and Research
      • Division of Hematology
      Scottsdale, AZ, United States
  • 2001–2005
    • Universität zu Lübeck
      • Institut für Pathologie
      Lübeck, Schleswig-Holstein, Germany
  • 2000
    • Universitätsklinikum Tübingen
      Tübingen, Baden-Württemberg, Germany
  • 1996
    • University of Salzburg
      Salzburg, Salzburg, Austria