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Rotraud Wieser
Ao.Univ.-Prof. Mag. Dr. Rotraud Wieser

Department of Medicine I (Division of Oncology)
Position: Associate Professor

ORCID: 0000-0003-4384-6658
T +43 1 40400 73779
rotraud.wieser@meduniwien.ac.at

Keywords

All-trans retinoic acid ; Chemotherapy resistance; EVI1; Leukemia, Myeloid, Acute; leukemic stem cells; miRNA; Transcription regulation

Research group(s)

Research interests

Most patients suffering from acute myeloid leukemia (AML) initially respond well to chemotherapy and achieve a complete remission. However, the majority of them eventually experience relapse, a stage of increased therapy resistance at which cure is rarely achieved. Specific genetic or gene expression alterations present in the bulk of the leukemic cells at diagnosis influence therapy responsiveness and predict patient survival. In addition, selective pressure exerted by chemotherapy leads to the accumulation of additional alterations that may contribute to therapy resistance at relapse.

Among the genes whose overexpression at diagnosis confers a poor prognosis is EVI1, which codes for a transcription factor. Previous studies from the Wieser lab have shown that EVI1 interacts functionally with all-trans retinoic acid (atRA), an agent used in the therapy of specific subtypes of AML. Current work addresses the interaction between EVI1 and atRA in leukemic stem cells, the cell type thought to represent the therapy resistant source of relapse.

A second project addresses the role of a G-protein coupled receptor, which is up-regulated at relapse of AML as compared to diagnosis, in cellular therapy resistance. Both lines of research aim at the identification of treatment modalities improving the survival of patients with AML.

Grants

  • Functional characterization of a receptor protein associated with poor therapy response and relapse of acute myeloid leukemia (2015)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Functional interactions between EVI1 and atRA in LSCs (2015)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Modulation of ATRA regulated transcription by EVI1 (2009)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Target genes of the MDS-associated transcription factor EVI 1 (Responsible) (2008)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Functions of the oncogene EVI1 in primary human CD34+ cells (2007)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Regulation of the EVI1 gene through 5´-end variability (2004)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • The leukemogenic transcription factor EVI1 and its putative antagonist, MDSu/EVI1: Expression patterns, biological properties and search for target genes (2002)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Investigations on the molecular consequences of chromosome 3q aberrations in myeloid Leukemia (Responsible) (2000)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Project
    Principal Investigator

Selected publications

  1. Konrad, T.A. et al., 2009. Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes. Journal of Leukocyte Biology, 86(4), pp.813-822. Available at: http://dx.doi.org/10.1189/jlb.0109042.
  2. Rommer, A. et al., 2013. Overexpression of primary microRNA 221/222 in acute myeloid leukemia. BMC Cancer, 13(1), p.364. Available at: http://dx.doi.org/10.1186/1471-2407-13-364.
  3. Steinmetz, B. et al., 2014. The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid . Cell Cycle, 13(18), pp.2931-2943. Available at: http://dx.doi.org/10.4161/15384101.2014.946869.
  4. Hackl, H. et al., 2015. A gene expression profile associated with relapse of cytogenetically normal acute myeloid leukemia is enriched for leukemia stem cell genes. Leukemia & Lymphoma, 56(4), pp.1126-1128. Available at: http://dx.doi.org/10.3109/10428194.2014.944523.
  5. Fisser, M.C. et al., 2014. Induction of the proapoptotic tumor suppressor gene Cell Adhesion Molecule 1 by chemotherapeutic agents is repressed in therapy resistant acute myeloid leukemia . Molecular Carcinogenesis, 54(12), pp.1815-1819. Available at: http://dx.doi.org/10.1002/mc.22252.