Publications (74)229.87 Total impact
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Article: International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) & European Competence Network on Mastocytosis (ECNM) consensus response criteria in advanced systemic mastocytosis.
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ABSTRACT: Systemic mastocytosis (SM) is characterized by accumulation of neoplastic mast cells and is leukemia (MCL), and SM associated with a myeloid neoplasm wherein one or both disease compartments exhibit advanced features. These variants, henceforth collectively referred to as 'advanced SM' for the purposes of this report, are typically characterized by organ damage and shortened survival. In contrast to indolent SM, where symptoms are usually managed by non-cytotoxic anti-mediator therapy, cytoreduction is usually necessary for disease control in advanced SM. Unfortunately, current drug treatment for these patients rarely results in complete clinical and histopathological remissions or improved survival. Previously defined response criteria were adapted to the heterogeneous presentations of advanced SM and the limited effects of available drugs. However, recent advances in understanding the molecular pathogenesis of SM and the corresponding prospect in targeted therapy make it a high priority to modify these criteria. The current document is the product of an international group of experts and summarizes the challenges in accomplishing this task and forwards a new proposal for response criteria, which builds upon prior proposals and should facilitate response evaluation in clinical trials.Blood 01/2013; · 9.90 Impact Factor -
Article: ICON: Eosinophil Disorders.
World Allergy Organization Journal 12/2012; 5(12):174-181. -
Article: Small-molecule inhibition of BRD4 as a new potent approach to eliminate leukemic stem- and progenitor cells in acute myeloid leukemia AML.
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ABSTRACT: Acute myeloid leukemia (AML) is a life-threatening stem cell disease characterized by uncontrolled proliferation and accumulation of myeloblasts. Using an advanced RNAi screen-approach in an AML mouse model we have recently identified the epigenetic 'reader' BRD4 as a promising target in AML. In the current study, we asked whether inhibition of BRD4 by a small-molecule inhibitor, JQ1, leads to growth-inhibition and apoptosis in primary human AML stem- and progenitor cells. Primary cell samples were obtained from 37 patients with freshly diagnosed AML (n=23) or refractory AML (n=14). BRD4 was found to be expressed at the mRNA and protein level in unfractionated AML cells as well as in highly enriched CD34+/CD38- and CD34+/CD38+ stem- and progenitor cells in all patients examined. In unfractionated leukemic cells, submicromolar concentrations of JQ1 induced major growth-inhibitory effects (IC50 0.05-0.5 µM) in most samples, including cells derived from relapsed or refractory patients. In addition, JQ1 was found to induce apoptosis in CD34+/CD38- and CD34+/CD38+ stem- and progenitor cells in all donors examined as evidenced by combined surface/Annexin-V staining. Moreover, we were able to show that JQ1 synergizes with ARA-C in inducing growth inhibition in AML cells. Together, the BRD4-targeting drug JQ1 exerts major anti-leukemic effects in a broad range of human AML subtypes, including relapsed and refractory patients and all relevant stem- and progenitor cell compartments, including CD34+/CD38- and CD34+/CD38+ AML cells. These results characterize BRD4-inhibition as a promising new therapeutic approach in AML which should be further investigated in clinical trials.Oncotarget 11/2012; · 4.78 Impact Factor -
Article: European Competence Network on Mastocytosis (ECNM): 10-year jubilee, update, and future perspectives.
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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.Wiener klinische Wochenschrift 11/2012; · 0.81 Impact Factor -
Article: Eosinophil, basophil, and mast cell infiltrates in the bone marrow: crossing the boundaries of diagnosis
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ABSTRACT: An increase in eosinophils, basophils, and/or mast cells in the bone marrow may pose considerable diagnostic problems for the hematopathologist. In a first step, it is crucial to classify these changes as either being reactive or neoplastic. A slight increase in eosinophils is often seen in reactive states of myeloid hyperplasia while an increase in basophils is usually indicative of a neoplastic hematologic disorder. Regarding mast cells, the presence of compact infiltrates is the major criterion for systemic mastocytosis whereas a diffuse interstitial increase is often encountered in reactive states of mast cell hyperplasia. When a neoplastic disorder is diagnosed, definitive classification depends on immunohistochemical, molecular, and cytogenetic markers. The use of a limited panel of antibodies against basophil-, eosinophil-, and mast cell-related antigens like 2D7, eosinophil major basic protein, tryptase, and CD117 (KIT) is sufficient to identify diffuse or compact infiltrates and to provide semiquantitative analysis of accumulations of neoplastic or reactive cells. We therefore recommend the use of such markers which may increase the value of hematopathologic investigations and thereby are of major help to improve diagnosis and prognostication in these patients. KeywordsBasophilic leukemia–Basophils–Bone marrow–Eosinophilic leukemia–Eosinophils–Mast cells–Mastocytosis–Myeloproliferative neoplasm with eosinophilia–Systemic mastocytosis04/2012; 4(2):101-111. -
Article: Pathogenesis and classification of eosinophil disorders: a review of recent developments in the field.
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ABSTRACT: Eosinophils and their products play an essential role in the pathogenesis of various reactive and neoplastic disorders. Depending on the underlying disease, molecular defect and involved cytokines, hypereosinophilia may develop and may lead to organ damage. In other patients, persistent eosinophilia is accompanied by typical clinical findings, but the causative role and impact of eosinophilia remain uncertain. For patients with eosinophil-mediated organ pathology, early therapeutic intervention with agents reducing eosinophil counts can be effective in limiting or preventing irreversible organ damage. Therefore, it is important to approach eosinophil disorders and related syndromes early by using established criteria, to perform all appropriate staging investigations, and to search for molecular targets of therapy. In this article, we review current concepts in the pathogenesis and evolution of eosinophilia and eosinophil-related organ damage in neoplastic and non-neoplastic conditions. In addition, we discuss classifications of eosinophil disorders and related syndromes as well as diagnostic algorithms and standard treatment for various eosinophil-related disorders.Expert Review of Hematology 04/2012; 5(2):157-76. · 1.16 Impact Factor -
Article: Controversies and open questions in the definitions and classification of the hypereosinophilic syndromes and eosinophilic leukemias.
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ABSTRACT: Eosinophilia is frequently detectable in certain myeloid neoplasms and various reactive conditions, but it may also occur in the absence of an apparent underlying disease, or, rarely, as a paraneoplastic feature with solid tumors. In myeloid neoplasms, eosinophils are considered to belong to the malignant clone in most cases, whereas in all other conditions, eosinophilia is a reactive process triggered by eosinopoietic cytokines. Excessive accumulation of eosinophils, also termed hypereosinophilia (HE), is typically seen in eosinophilic leukemias, but it may also occur in other neoplasms and reactive disorders. HE-related end organ damage may develop in patients with reactive HE but also in those with hematologic malignancies. During the past few years, our knowledge about HE and HE-related organ damage in hematologic and nonhematologic disorders has improved considerably. Moreover, proposals for the definition and classification of eosinophil disorders have been generated by various expert groups and by the World Health Organization (WHO). However, several questions related to eosinophils and HE remain open, and many aspects of the definition and classification of eosinophil disorders and related pathologies remain controversial. In the current article, these open issues are discussed with special reference to the 2008 WHO classification of myeloid neoplasms and other classifications proposed by immunologists and various expert panels, as well as definitions and criteria recently proposed in a multidisciplinary consensus proposal.Seminars in Hematology 04/2012; 49(2):171-81. · 3.99 Impact Factor -
Article: Contemporary consensus proposal on criteria and classification of eosinophilic disorders and related syndromes.
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ABSTRACT: Eosinophilia is an important indicator of various neoplastic and nonneoplastic conditions. Depending on the underlying disease and mechanisms, eosinophil infiltration can lead to organ dysfunction, clinical symptoms, or both. During the past 2 decades, several different classifications of eosinophilic disorders and related syndromes have been proposed in various fields of medicine. Although criteria and definitions are, in part, overlapping, no global consensus has been presented to date. The Year 2011 Working Conference on Eosinophil Disorders and Syndromes was organized to update and refine the criteria and definitions for eosinophilic disorders and to merge prior classifications in a contemporary multidisciplinary schema. A panel of experts from the fields of immunology, allergy, hematology, and pathology contributed to this project. The expert group agreed on unifying terminologies and criteria and a classification that delineates various forms of hypereosinophilia, including primary and secondary variants based on specific hematologic and immunologic conditions, and various forms of the hypereosinophilic syndrome. For patients in whom no underlying disease or hypereosinophilic syndrome is found, the term hypereosinophilia of undetermined significance is introduced. The proposed novel criteria, definitions, and terminologies should assist in daily practice, as well as in the preparation and conduct of clinical trials.The Journal of allergy and clinical immunology 03/2012; 130(3):607-612.e9. · 9.17 Impact Factor -
Article: Advanced systemic mastocytosis as a mimicker of metastatic clear cell renal cell carcinoma.
Leukemia research 03/2012; 36(6):799-801. · 2.36 Impact Factor -
Article: Definitions, criteria and global classification of mast cell disorders with special reference to mast cell activation syndromes: a consensus proposal.
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ABSTRACT: Activation of tissue mast cells (MCs) and their abnormal growth and accumulation in various organs are typically found in primary MC disorders also referred to as mastocytosis. However, increasing numbers of patients are now being informed that their clinical findings are due to MC activation (MCA) that is neither associated with mastocytosis nor with a defined allergic or inflammatory reaction. In other patients with MCA, MCs appear to be clonal cells, but criteria for diagnosing mastocytosis are not met. A working conference was organized in 2010 with the aim to define criteria for diagnosing MCA and related disorders, and to propose a global unifying classification of all MC disorders and pathologic MC reactions. This classification includes three types of 'MCA syndromes' (MCASs), namely primary MCAS, secondary MCAS and idiopathic MCAS. MCA is now defined by robust and generally applicable criteria, including (1) typical clinical symptoms, (2) a substantial transient increase in serum total tryptase level or an increase in other MC-derived mediators, such as histamine or prostaglandin D(2), or their urinary metabolites, and (3) a response of clinical symptoms to agents that attenuate the production or activities of MC mediators. These criteria should assist in the identification and diagnosis of patients with MCAS, and in avoiding misdiagnoses or overinterpretation of clinical symptoms in daily practice. Moreover, the MCAS concept should stimulate research in order to identify and exploit new molecular mechanisms and therapeutic targets.International Archives of Allergy and Immunology 01/2012; 157(3):215-25. · 2.40 Impact Factor -
Article: Systemic mastocytosis.
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ABSTRACT: An unusual disease, mastocytosis challenges the pathologist with a variety of morphologic appearances and heterogeneous clinical presentations ranging from skin manifestations (pruritus, urticaria, dermatographism) to systemic signs and symptoms indicative of mast cell mediator release, including flushing, hypotension, headache, and anaphylaxis among others. In this article, we focus on recognizing the cytology, histopathology, clinical features, and prognostic implications of systemic mastocytosis, a clonal and neoplastic mast cell proliferation infiltrating extracutaneous organ(s) with or without skin involvement. Diagnostic pitfalls are reviewed with ancillary studies to help unmask the mast cell and exclude morphologic mimics.Hematology/oncology clinics of North America 10/2011; 25(5):1067-83, vii. · 2.05 Impact Factor -
Article: Idiopathic cytopenia of undetermined significance (ICUS) and idiopathic dysplasia of uncertain significance (IDUS), and their distinction from low risk MDS.
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ABSTRACT: It is now generally appreciated that hematologic neoplasms can develop over many years if not decades, often being initially occult or showing minimal (subdiagnostic) abnormalities. However, whereas such early neoplastic conditions have been defined in some detail in lymphoproliferative neoplasms, little is known about minimal lesions preceding the manifestation of an overt myeloid neoplasm, about underlying mechanisms, the clinical course and outcome, and the prognostic significance of such conditions. Members of several groups have recently described two 'premalignant' myeloid conditions, namely idiopathic cytopenia of undetermined significance (ICUS) and idiopathic bone marrow dysplasia of uncertain significance (IDUS). At least in some patients these are neoplastic conditions. Both conditions may progress to an overt myelodysplastic syndrome (MDS), but may also progress to another myeloid neoplasm such as acute myeloid leukemia, a myeloproliferative neoplasm (MPN), or a mast cell disorder (mastocytosis). In ICUS the dysplasia is mild and does not fulfill the WHO criteria for MDS but cytopenias can be severe. In IDUS the dysplasia is prominent but cytopenias, if detectable, are mild. In both conditions it is possible that a neoplastic clone has already replaced most or all of normal bone marrow cells when ICUS or IDUS is detected, but evidence to support this possibility is not necessarily available. For both groups of patients we recommend a thorough hematologic follow up because of the potential of disease-manifestation and the unpredictable form and time of progression. In the present review, we discuss current concepts relating to ICUS and IDUS as well as diagnostic approaches and available criteria.Leukemia research 09/2011; 36(1):1-5. · 2.36 Impact Factor -
Article: KIT-D816V-independent oncogenic signaling in neoplastic cells in systemic mastocytosis: role of Lyn and Btk activation and disruption by dasatinib and bosutinib.
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ABSTRACT: Systemic mastocytosis (SM) either presents as a malignant neoplasm with short survival or as an indolent disease with normal life expectancy. In both instances, neoplastic mast cells (MCs) harbor D816V-mutated KIT, suggesting that additional oncogenic mechanisms are involved in malignant transformation. We here describe that Lyn and Btk are phosphorylated in a KIT-independent manner in neoplastic MCs in advanced SM and in the MC leukemia cell line HMC-1. Lyn and Btk activation was not only detected in KIT D816V-positive HMC-1.2 cells, but also in the KIT D816V-negative HMC-1.1 subclone. Moreover, KIT D816V did not induce Lyn/Btk activation in Ba/F3 cells, and deactivation of KIT D816V by midostaurin did not alter Lyn/Btk activation. siRNAs against Btk and Lyn were found to block survival in neoplastic MCs and to cooperate with midostaurin in producing growth inhibition. Growth inhibitory effects were also obtained with 2 targeted drugs, dasatinib which blocks KIT, Lyn, and Btk activation in MCs, and bosutinib, a drug that deactivates Lyn and Btk without blocking KIT activity. Together, KIT-independent signaling via Lyn/Btk contributes to growth of neoplastic MCs in advanced SM. Dasatinib and bosutinib disrupt Lyn/Btk-driven oncogenic signaling in neoplastic MC, which may have clinical implications and explain synergistic drug interactions.Blood 06/2011; 118(7):1885-98. · 9.90 Impact Factor -
Article: Clinical and laboratory parameters of mast cell activation as basis for the formulation of diagnostic criteria.
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ABSTRACT: 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.International Archives of Allergy and Immunology 05/2011; 156(2):119-27. · 2.40 Impact Factor -
Chapter: Diagnostic Criteria and Classification of Myelodysplastic Syndromes
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ABSTRACT: A classification for myelodysplastic syndromes (MDS) has been proposed by several working groups and the World Health Organization (WHO). The recently updated criteria of the WHO are useful for discriminating MDS variants from each other. Moreover, minimal diagnostic criteria for MDS have been defined. In a few patients with unexplained cytopenia or dysplasia these criteria are not met. For these patients, the terms idiopathic cytopenia of unknown significance (ICUS) and idiopathic dysplasia of unknown significance (IDUS) have been proposed. Both conditions may progress to overt MDS over time. Therefore, once diagnosed, these patients should have a hematologic follow up. The final diagnosis of MDS has to be based on defined criteria and exclusion of all other causes of cytopenia and dysplasia, which requires detailed and sometimes extensive investigations, including a bone marrow biopsy, immunohistochemical studies, cytogenetic analysis, molecular studies, and flow cytometry. A diagnostic challenge is the potential co-existence of two myeloid neoplasms producing cytopenia or/and dysplasia in one patient. Once diagnosed, patients with MDS should be classified according to FAB and WHO criteria, and their risk concerning survival and AML evolution should be estimated by employing patient-related and disease-related risk factors, and established scoring systems, including the IPSS and/or WPSS, both of which are global standard. KeywordsMDS-Diagnostic criteria-ICUS-IDUS-IPSS03/2011: pages 43-53; -
Article: Classification and response criteria in mast cell disorders: time to revise?
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ABSTRACT: No abstract available.International Archives of Allergy and Immunology 02/2011; 155(3):306-8. · 2.40 Impact Factor -
Article: Mast cell hyperplasia, B-cell malignancy, and intestinal inflammation in mice with conditional expression of a constitutively active kit.
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ABSTRACT: Signaling through the receptor tyrosine kinase kit controls proliferation and differentiation of hematopoietic precursor cells and mast cells. Somatic point mutations of the receptor that constitutively activate kit signaling are associated with mastocytosis and various hematopoietic malignancies. We generated a Cre/loxP-based bacterial artificial chromosome transgenic mouse model that allows conditional expression of a kit gene carrying the kitD814V mutation (the murine homolog of the most common mutation in human mastocytosis, kitD816V) driven by the kit promoter. Expression of the mutant kit in cells of adult mice, including hematopoietic precursors, caused severe mastocytosis with 100% penetrance at young age frequently associated with additional hematopoietic (mostly B lineage-derived) neoplasms and focal colitis. Restriction of transgene expression to mature mast cells resulted in a similar mast cell disease developing with slower kinetics. Embryonic expression led to a hyperproliferative dysregulation of the erythroid lineage with a high rate of perinatal lethality. In addition, most adult animals developed colitis associated with mucosal mast cell accumulation. Our findings demonstrate that the effects of constitutive kit signaling critically depend on the developmental stage and the state of differentiation of the cell hit by the gain-of-function mutation.Blood 02/2011; 117(6):2012-21. · 9.90 Impact Factor -
Article: Polo-like kinase-1 as a novel target in neoplastic mast cells: demonstration of growth-inhibitory effects of small interfering RNA and the Polo-like kinase-1 targeting drug BI 2536.
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ABSTRACT: In advanced systemic mastocytosis the response of neoplastic mast cells to conventional drugs is poor and the prognosis is bad. Current research is, therefore, attempting to identify novel drug targets in neoplastic mast cells. Polo-like kinase-1 is a serine/threonine kinase that plays an essential role in mitosis and has recently been introduced as a new target in myeloid leukemias and solid tumors. In the present study, we analyzed the expression and function of Polo-like kinase-1 in neoplastic mast cells in systemic mastocytosis. As determined by immunostaining, primary neoplastic mast cells as well as the human mast cell leukemia cell line HMC-1 displayed phosphorylated Polo-like kinase-1. In addition, neoplastic mast cells expressed Polo-like kinase-1 mRNA. Polo-like kinase-1-specific small interfering RNA induced apoptosis in neoplastic mast cells, whereas no effect was seen with a control small interfering RNA. BI 2536, a drug targeting Polo-like kinase-1, was found to inhibit proliferation in HMC-1 cells in a dose-dependent manner. BI 2536 also inhibited the growth of primary neoplastic mast cells and cells of the canine mastocytoma cell line C2. The growth-inhibitory effects of BI 2536 on neoplastic mast cells were found to be associated with mitotic arrest and subsequent apoptosis. Finally, BI 2536 was found to synergize with the KIT-targeting kinase inhibitor midostaurin (PKC412) in inhibiting the growth of neoplastic mast cells. In control experiments, BI 2536 did not induce apoptosis in normal cultured mast cells. Collectively, our data show that Polo-like kinase-1 is a potential therapeutic target in neoplastic mast cells. Targeting Polo-like kinase-1 may be an attractive pharmacological concept in the management of advanced systemic mastocytosis.Haematologica 01/2011; 96(5):672-80. · 6.42 Impact Factor -
Article: Systemic mastocytosis (SM) and associated malignant bone marrow histiocytosis - a hitherto undescribed form of SM-AHNMD.
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ABSTRACT: An elderly woman presented with anaemia, thrombocytopenia and multifocal lytic and sclerotic bone lesions. Trephine bone marrow biopsy demonstrated widespread involvement by systemic mastocytosis (SM). The neoplastic mast cells expressed mast cell tryptase, CD117, CD25 and CD9, and were accompanied by compact sheets of atypical large histiocytic cells, expressing CD68, CD4, S-100 protein and CD14, in keeping with a concomitant histiocytosis (SM-AHNMD). Mutation analysis revealed the activating point mutation D816V of the c-kit proto-oncogene in microdissected pooled bone marrow mast cells. Partial remission was achieved using interferon alpha. To the best of our knowledge this is the first reported case of SM-AHNMD with histiocytosis as the non-mast cell component.Polish journal of pathology: official journal of the Polish Society of Pathologists 01/2011; 62(2):101-4. · 0.35 Impact Factor -
Article: Aberrant expression of CD30 in aggressive systemic mastocytosis and mast cell leukemia: a differential diagnosis to consider in aggressive hematopoietic CD30-positive neoplasms.
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ABSTRACT: During the past two decades the immunophenotype of normal, reactive, and neoplastic mast cells (MCs) has been established. These studies have convincingly demonstrated that MCs form a separate lineage within the myeloid cell family. A most intriguing finding was that in contrast to normal MCs, neoplastic MCs in systemic mastocytosis (SM) aberrantly express several lymphoid marker antigens such as CD2 and CD25. This phenomenon has now been topped by the unexpected observation that neoplastic MCs in aggressive variants of SM and MC leukemia (leukemic variant of SM) aberrantly express CD30, whereas this antigen, Ki-1, is not detectable or is expressed only weakly in MCs in most patients with indolent SM. These observations may have implications for the evolution of SM as well as for diagnostic evaluation and grading in these patients. Moreover, these observations suggest that advanced SM has to be considered as a differential diagnosis of CD30-positive lymphoid neoplasms. Finally, CD30 may be considered as a potential target of antibody-based therapeutic intervention in advanced mast cell disorders.Leukemia & lymphoma 01/2011; 52(5):740-4. · 2.40 Impact Factor
Top co-authors
Top Journals
Institutions
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2013
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Stanford Medicine
Stanford, CA, USA
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2012
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Ludwig Boltzmann-Cluster Oncology (LB-CO) | Medical University Vienna
Vienna, Vienna, Austria
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2004–2012
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Medical University of Vienna
- Institut für Sozialmedizin
Vienna, Vienna, Austria
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2011
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Stanford University
- Department of Pathology
Stanford, CA, USA -
The Bracton Centre, Oxleas NHS Trust
Dartford, ENG, United Kingdom
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2010
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Ludwig-Maximilian-University of Munich
- Institute of Pathology
München, Bavaria, Germany
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2002–2008
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Eberhard-Karls-Universität Tübingen
- Institute of Pathology and Neuropathology
Tübingen, Baden-Wuerttemberg, Germany
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2006
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Universität Hamburg
- Department of Pathology
Hamburg, Hamburg, Germany
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2005–2006
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Universitätsklinikum Schleswig - Holstein
Kiel, Schleswig-Holstein, Germany
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2002–2005
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Universität zu Lübeck
- Institut für Pathologie
Lübeck, Schleswig-Holstein, Germany
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2002–2004
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University of Vienna
- Universitätsklinik für Innere Medizin I
Vienna, Vienna, Austria
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