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You are here: FRIAS Fellows Fellows 2016/17 Dr. Miriam Erlacher

Dr. Miriam Erlacher

Every year, approximately 50 Fellows are invited to work on their projects at FRIAS for 2 to 12 months in an intellectually stimulating environment. Fellows that have already been at FRIAS before can return to FRIAS for 2 to 6 weeks within the framework of the Alumni Programme, for example in order to finish a project. Furthermore, junior and senior researchers are regularly invited as guest researchers.

Schätz

Our Research Focus profited enormously from the international team of Fellows and guest researchers at FRIAS.

Prof. Dr. Tobias Schätz, ERC Consolidator Grant 2015, Research Focus Quantum Transport 2014/15

University Hospital of Freiburg
Pediatric hematology and oncology/Pediatric immunology/Stem cell biology/Apoptosis signaling
Junior Fellow
October 2013 - July 2014

CV

Born 1978 in Bozen, Italy; 1997-2003 medical school, Leopold-Franzens University in Innsbruck, Austria; 2000-2002 MD thesis on “Reciprocal action between T cell receptor and gluco-cocorticoid receptor induced apoptosis in murine thymocytes” at the Institute of Experimental Pathophysiology and Immunology, supervised by Prof. Dr. G. Wick and Dr. Jan Wiegers; 2003 degree Dr.med.univ. (MD) at the University Innsbruck. 2003-2006 PhD studies in the program „Molecular Oncology“ at the Innsbruck Medical University (“The role of the BH3-only proteins Bim and PUMA in development and cell death signaling”, supervised by Prof. Dr. Andreas Villunger); 2007 “MD/PhD” at the Innsbruck Medical University, passed with distinction.

04-06/2006 Internship („Tirocinio“) at the Hospital of Sterzing (Italy); 07.08.2006 License to practice medicine (“Approbation”), University of Bologna (Italy). 2006-2013 Resident at the Division of Pediatric Hematology and Oncology, Department of Pediatrics and Adolescent Medicine, University of Freiburg; since 10/08 Junior group leader, with supervision of MD and PhD students. 2009-2013 Fellowship holder within the “Margarete-von-Wrangell Habilitationsprogramm” (Ministerium für Wissenschaft, Forschung und Kunst Baden-Württemberg and European Social Fund (ESF)). 03/2013 Board examination in pediatric and adolescent medicine. Since 03/2013 Fellow in Pediatric Hematology and Oncology, Department of Pediatrics and Adolescent Medicine, University of Freiburg, Germany.

 

Selected Publications

  • Labi V, Bertele D, Woess C, Tischner D, Bock FJ, Schwemmers S, Pahl HL, Geley S, Kunze M, Niemeyer CM, Villunger AV and Erlacher M. Haematopoietic Stem Cell Survival and Transplantation Efficacy is Limited by the BH3-only Proteins Bim and Bmf. EMBO Mol. Med. 2013 Jan;5(1):122-36. doi:
  • Labi V, Erlacher M, Krumschnabel G, Manzl C, Tzankov A, Pinon J, Egle A, Villunger A.
    Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation. Genes Dev. 2010 Aug 1;24(15):1602-7.
  • Niemeyer CM, Kang MW, Shin DH, Furlan I, Erlacher M, Bunin NJ, Bunda S, Finklestein JZ, Sakamoto KM, Gorr TA, Mehta P, Schmid I, Kropshofer G, Corbacioglu S, Lang PJ, Klein C, Schlegel PG, Heinzmann A, Schneider M, Starý J, van den Heuvel-Eibrink MM, Hasle H, Locatelli F, Sakai D, Archambeault S, Chen L, Russell RC, Sybingco SS, Ohh M, Braun BS, Flotho C, Loh ML. Germline CBL mutations cause developmental abnormalities and predispose to juvenile myelomonocytic leukemia. Nat Genet. 2010 Aug 8.
  • Erlacher M, Labi V, Böck G, Tzankov A, Strasser A, Villunger A. Combined loss of Bim and Puma mirrors the effects of Bcl-2 overexpression in some but not all forms of cell death. J Exp Med. 2006 Dec 25;203(13):2939-51.
  • Erlacher M, Michalak EM, Kelly PN, Labi V, Niederegger H, Coultas L, Adams JM,
    Strasser A, Villunger A. The BH3-only proteins PUMA/bbc3 and Bim are rate-limiting for γ-radiation and glucocorticoid induced apoptosis of lymphoid cells in vivo. Blood. 2005 Aug 23; 2005 Dec 15;106(13):4131-8.

 

FRIAS Research Project

Characterization of survival signals essentially required for maintenance of human hematopoiesis

Myelosuppression is a frequent and often dose-limiting side effect of anticancer therapy and associated with significant treatment-related morbidity. Since most chemotherapeutic regimens rely on full hematopoietic regeneration after transient aplasia, a better knowledge of human hematopoietic stem cells and their “minimal requirements” to survive and to maintain or regenerate the hematopoietic system is required. Thus, we here aim to identify proteins and signaling pathways essentially required for stem cell survival.
Based on data from mouse models it is anticipated, but far from proven, that the pro-survival Bcl-2 family members Bcl-xL and Mcl-1 are essential genes for hematopoietic stem and progenitor cells (HSPCs) also in humans. Given the intense efforts aiming to develop selective inhibitors of pro-survival Bcl-2 family members, i.e. so-called BH3-mimetics, it is essential to define the particular vulnerabilities of human HSPCs to the inhibition of individual Bcl-2 family proteins, either per se, or in combination with frequently used anticancer agents.
By using RNAi based ablation of gene expression in cord blood-derived CD34+ cells we will study, which single pro-survival Bcl-2 proteins or combinations thereof are essential for human HSPC survival, and which upstream signaling pathways contribute to their expression. Additionally, by simultaneous inhibition of their antagonists, the BH3-only proteins, we intend to rescue CD34+ cells from death, thereby identifying BH3-only proteins critically harming HSCPs.