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Department of Internal Medicine


  • ACCESS POINT Oncology

    Molecular oncology research to develop new treatment strategies based on clinical (OIS) and biological (biobank) datasets

    • Project Number: K3- F-730/003-2020
    • Project Lead: Klaus Podar, Karl Landsteiner University of Health Sciences / Molecular Oncology / Hematology
    • Project Partner: Karl Landsteiner University of Health Sciences / Division of Internal Medicine 2 (University Hospital Krems), Karl Landsteiner University of Health Sciences / Division of Pharmakologie, FH St. Pölten / Institute for IT Security Research, MedAustron
    • Duration: 48 months starting from 01.01.2020
  • Biomarker- based therapeutic prevention

    Biomarker- based therapeutic prevention of bone metastases in breast cancer: Defining the pathophysiologic impact of the endosteal niche

    • Project Number: LSC18_010
    • Project Lead: Sonia Vallet, Karl Landsteiner University of Health Sciences / Molecular Oncology / Hematology, Sonia Vallet, Karl Landsteiner University of Health Sciences / Division of Internal Medicine 2 (University Hospital Krems)
    • Project Partner: IMC University of Applied Sciences Krems / Department of Life Sciences
    • Duration: 36 months starting from 01.12.2019


    Breast cancer (BC) is the most common malignancy in women. Most of the tumors are detected at early stages and treated with curative intent. However, up to one third of patients relapse, of which 70% develop bone metastases with survival rates dropping under 10% at 5 years. Efforts to find markers of bone metastases development have so far failed, mainly due to the poor understanding of early pathogenetic steps. Therefore, there remains a need for biomarkers that identify patients at high risk for bone metastases. In addition, despite the frequency of skeletal involvement and the associated morbidity and mortality, effective strategies to prevent bone metastases are lacking. Previous studies identified the endosteum as site of entry for bone metastatic BC cells, where OBs regulate tumor cell migration and survival. Specifically, our own data suggest a key role for pre-OBs in BC bone colonization. Here, I propose to unravel the pathophysiologic role of the endosteal niche, OB lineage cells in particular, during early phases of BM in BC by generating innovative in vitro models of OB differentiation.

  • High Content Imaging

    High-content optical imaging to decode human immune cell interactions in health and allergic disease

    • Project Number: LSC18_022
    • Project Lead: Johann Danzl, IST Austria
    • Project Partner: Stanford University / Department of Pathology, Karl Landsteiner University of Health Sciences / Division of Internal Medicine 2 (University Hospital St. Pölten), Karl Landsteiner University of Health Sciences / Division of Otorhinolaryngology (University Hospital St. Pölten)
    • Duration: 36 months starting from 01.12.2019


    Allergic disease is a clinical and societal burden in Lower Austria and elsewhere. Severe food allergy can manifest as anaphylactic reaction with potentially fatal outcome. IgE-mediated food allergy in children is increasing, affecting 3-8% of under 4 year olds, with peanut as most common specificity. IgE-producing B-cells and IgE-primed mast cells are critical to TH2 driven, Type I hypersensitivity allergic reactions, but the full scope of altered immunity in these patients and the basis for oral immunotherapy efficacy are unknown, particularly in the solid tissues of the human body.
    Here, we propose to analyze the cellular organization of the human immune system in health and allergic disease. Our interdisciplinary consortium consists of Dr. Danzl (IST) providing optical imaging, Dr. Boyd (Stanford) contributing immunology expertise, and clinical partners Dr. Maieron and Dr. Sprinzl (St. Pölten) providing human patient tissue biopsies to link our scientific findings to the clinic.
    We will further develop imaging technology to characterize transcriptional profiles of single cells in native tissue context. This identifies cell types, subtypes, and activation states, as well as their spatial arrangements and interactions. We will define molecularly-informed cellular microenvironments or “tissue niches” by detecting hundreds to thousands of different mRNAs in highly multiplex single-molecule RNA fluorescence in situ hybridization. We will also develop multiplex protein imaging, with the same goal of decoding patterns of spatial relationships.
    We will verify detection of known spatial organization features in human tonsils and Peyer’s patches. We will then extract novel information by defining cell type specific “interactomes” and specific microenvironments or niches based on detailed molecular and spatial information in our multiplex imaging.
    We then focus on gastrointestinal (GI) mucosa-associated immune cells and characterize microenvironments of lymphocytes and effector cells. We emphasize IgE-producing B-cells/plasma cells, and evaluate how their microenvironments differ from those of B-cells and plasma cells producing other antibody isotypes, such as IgA or IgG4. The latter may serve a protective role against allergic disease.
    We translate these scientific questions to the clinic by multiplex analysis of patient GI biopsies from a Stanford peanut allergy immunotherapy trial. We hypothesize that not only abundance and location of specific isotype-producing B-cells are shifted in allergy but that specific microenvironments act as major drivers of disease and therapeutic responses.
    Multiplex single cell analysis of GI biopsies of the same patients pre and post oral immunotherapy will identify therapy-related changes in cellular composition, phenotype, and tissue architecture. We propose to define
    multi-parameter, spatially informed biopsy biomarkers predictive of treatment response as basis for a personalized medicine approach to immunotherapy.

  • JunB in multiple myeloma

    Pathophysiological role of JunB in multiple myeloma

    • Project Number: WST3-F-5031298/002-2018
    • Project Lead: Klaus Podar, Karl Landsteiner University of Health Sciences / Molecular Oncology / Hematology, Klaus Podar, Karl Landsteiner University of Health Sciences / Division of Internal Medicine 2 (University Hospital Krems)
    • Project Partner: The Antibody Lab GmbH, IMC University of Applied Sciences Krems, University of Veterinary Medicine Vienna / Institute for Pharmacology and Toxicology
    • Duration: 36 months starting from 01.10.2018


    Dieses Projekt wird aus Mitteln des Europäischen Fonds für regionale Entwicklung (EFRE) kofinanziert. Nähere Informationen zu IWB/EFRE finden Sie auf www.efre.gv.at
    Microenvironment-induced signaling pathways regulate the activity of numerous transcription factors (TFs). Approaches to target TFs are among the most promising novel anticancer strategies with a potentially high therapeutic index. Our recent data indicated a key role for the AP-1 family member JunB in MM pathogenesis (Fan et al., Leukemia 2017). In continuation of these findings, the proposed project aims to further define JunB as a novel therapeutic target in MM, and to thereby set the pace for the development of direct or indirect JunB inhibitors in order to further improve patient outcome.

  • MFSD1 Transporter

    Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis

    • Project Number: LSC16_021
    • Project Lead: Daria Siekhaus, IST Austria
    • Project Partner: Karl Landsteiner University of Health Sciences / Division of Internal Medicine 1 (University Hospital St. Pölten)
    • Duration: 36 months starting from 01.08.2017


    Metastatic spread causes 90% of all tumor related fatalities and thus represents the greatest challenge for cancer patient survival. Tumor cells need to become motile and cross vascular barriers for metastatic spread. How these processes are controlled is not yet fully understood. The laboratory of Dr. Daria Siekhaus has identified a novel transporter, CG8602, required for Drosophila macrophages to invasively migrate into the tissues of the embryonic germband. Data from the Siekhaus lab point towards a role for CG8602 in regulating the glycosylation and stability of proteins that limit tissue entry. CG8602 appears necessary for the increased level of T antigen present on the surface of macrophages invading the tissue of the germband. Intriguingly, increased levels of T antigen have been found in metastatic cancer and antibodies against T antigen can reduce metastasis. This raised our interest in translating our findings into vertebrates, and Dr. Siekhaus recruited a post-doctoral fellow, Dr. Marko Roblek, with extensive experience in studying metastasis in mice back to Austria from Switzerland. This fellowship will help pay for his salary and material costs and thus enable him to conduct the work that will form the foundation for establishing his own independent lab. The mammalian ortholog of the CG8602 transporter, called MFSD1, is highly conserved, and belongs to the solute carrier superfamily (SLC). Yet its functions remain unknown due to a lack of prior studies. We seek to examine the role of MFSD1 in tumor cells during mouse metastatic initiation, We also will examine whether and how MFSD1 is involved in regulating protein glycosylation, protein stability, and how these potential changes affect the regulation of invasive tumor migration. By analyzing the function of MFSD1 and its interaction partners we aim to uncover the mechanism from aberrant glycosylation to the invasive migration phenotype observed during metastatic spread of tumors. This will include analysis of cell surface proteins, signaling cascades, and transcriptional regulation of cell migration. To test the relevance of these findings for the clinic, we are partnering with Dr. Wiesholzer and Dr. Kitzwoegerer at the Clinical Division for Internal Medicine, KLU University St Poelten. By analyzing resected tumor tissue from patients we will determine whether the level or localization of MFSD1 can be correlated with disease prognosis. We are eager to transfer findings from Drosophila to the vertebrate system in the context of metastasis research. Our prior data leads us to believe that this will lead to the description of an evolutionarily conserved mechanism that regulates invasive migration regulation from fly to vertebrates. This work can lay the ground work for
    understanding the basic biology of a novel vertebrate gene involved in regulating invasion and metastasis, and thus for the eventual development of a new therapeutic target and diagnostic biomarker for the clinic.

  • Tumor Cachexia

    Metabolic characterization of chronic inflammatory conditions such as metabolic syndrome and tumor cachexia

    • Project Number: LSC14_021
    • Project Lead: Martin Pecherstorfer, Karl Landsteiner University of Health Sciences / Division of Internal Medicine 2 (University Hospital Krems)
    • Project Partner: IMC University of Applied Sciences Krems / Applied Bioanalytics & Drug Development, University of Vienna / Department of Analytical Chemistry, Medical University Graz / Core Facility Mass Spectrometry, Medical University of Vienna / Institute of Medical Statistics, Rudolfstiftung Hospital / Karl Landsteiner Institute for Obesity and Metabolic Diseases
    • Duration: 54 months starting from 01.02.2016


    The clinical picture of the metabolic syndrome (MeS) is characterized by obesity, hypertension, insulin resistance and pathological blood lipid levels. Furthermore, the existence of a chronic inflammatory state in the adipose tissue leads to changes in the lipid metabolism of the fat cells. As a result, this leads to a disturbed uptake, deposition and release of lipids and free fatty acids. Interestingly, in the blood plasma of patients with tumor cachexia (CaC), lipid and inflammatory markers are similar to those of the metabolic syndrome. Tumor cachexia (CaC) is the term for a metabolic disorder that occurs as a result of cancer. This disorder leads to cachexia of the patient and emaciation.
    For research, this raises two important questions: What are the pathophysiological processes in the metabolic syndrome and the tumor syndrome cachexia? Is there a common biological marker for the pathophysiological processes in metabolic syndrome and tumor cachexia?


  1. 17 Sep

    International Skills Lab Symposium 2020

    17. September 2020, 09:00 - 19. September 2020, 18:00
    Karl Landsteiner Privatuniversität für Gesundheitswissenschaften, Skills Lab, Trakt Y
  2. 14 Mar

    Open House - March 2020 - CANCELLED

    14. March 2020, 10:00 - 14:00
    Karl Landsteiner University, Dr.-Karl-Dorrek-Straße 30,3500 Krems, Trakt Y, Erdgeschoß
  3. 27 Feb

    Neurophysiology symposium: Ion channels in nerve cells and associated diseases

    27. February 2020, 15:30 - 18:30
    Karl Landsteiner University of Health Sciences, Wing Y, Auditorium