Prof. Dr. Klaus-Michael Debatin

Director of the Department of Pediatrics and Adolescent Medicine
Ulm University Medical Center

Address: Eythstr. 24, 89075 Ulm, Germany

Secretariat: Susanne Glatzel, Bianca Welz
phone: +49-731-500-57001

e-mail: klaus-michael.debatin@uniklinik-ulm.de

1971 - 1978

Medical school, Universities of Ulm, Freiburg and Heidelberg

1979

Doctorate degree, University of Heidelberg

1979 - 1982

Research fellow/DFG scholarship holder, Institute of Immunology, University of Heidelberg and Max-Planck-Institute for Immunobiology, Freiburg

Between 1983 and 1991

Guest scientist at the German Cancer Research Center Heidelberg, the Dana-Farber Cancer Institute Boston, the Memorial Sloan-Kettering Cancer Center New-York, the Institute Mario Negri and the University Children's Hospital in Milan

1989

Board Certification as Medical Specialist in Pediatrics

1990

Habilitation

1991 - 1994

Heisenberg fellow of the German Research Foundation (DFG) at the National Cancer Institute of the U.S.A. (Fogarty Fellow), at the German Cancer Research Center Heidelberg and at Hôpital Necker, Paris

1994 - 1997

Head, Hematology/Oncology Section, University Children's Hospital Heidelberg

Since 1997

Full Professor and Director of the Department of Pediatrics and Adolescent Medicine, UIm University

Qualifications
  • Medical Specialist in Pediatrics
  • Focus on Pediatric Hematology and Oncology
  • Additional Qualification Allergology
Scientific Profile

Over the past decades cell death research and the clinical implications of cell death pathways for diseases and their therapeutic manipulation have been the major focus of the Debatin lab. The research of his lab covered several areas starting from the discovery of the CD95 death receptor and the CD95 system as a key apoptosis signaling pathway in 1989 via the first demonstration of apoptosis induction via physiological death system (CD95) in leukemia cells through the discovery of the participation of apoptosis signaling in anticancer therapy (1996) to recent work on understanding the role of apoptosis sensitivity and resistance for Graft-versus-Host-Disease (GvHD) and T-cell function (see Strauss group) as well as the prognostic impact of apoptosis sensitivity in pediatric leukemia and the development of appropriate mouse models for studying human acute lymphoblastic leukemia (see Meyer group).

A special focus within the different activities is on understanding mechanisms of sensitivity and resistance of tumor cells for anticancer therapy. This also includes the analysis of signaling pathways that may help to overcome resistance to molecular targeted therapy or conventional therapy using cytotoxic drugs and irradiation in human tumors with a particular focus on pediatric oncology. In addition to the focus on leukemia, leukemia models and neuroblastoma (see Beltinger group), glioblastoma is of particular interest (see Debatin/Westhoff group).

  1. Trauth BC, Klas C, Peters AMJ, Matzku S, Möller P, Falk W, Debatin KM, Krammer PH (1989): Monoclonal antibody-mediated tumor regression by induction of apoptosis. Science 245, 301-305.
    Discovery of the CD95 (APO-1/Fas) death receptor system
  2. Debatin KM, Goldmann CK, Bamford R, Waldmann TA, Krammer PH (1990): Monoclonal antibody-mediated apoptosis in adult T cell leukemia. Lancet 335, 497-500.
    First description of death receptor induced apoptosis in primary tumor cells
  3. Dhein J, Walczak H, Bäumler C, Debatin KM, Krammer PH (1995): Autocrine T-cell suicide mediated by APO-1/Fas (CD95). Nature 373, 438-441.
    Description of the mechanistic role of the CD95 system in T cell homeostasis
  4. Rieux-Laucat F, Le Deist F, Hivroz C, Roberts IAG, Debatin KM, Fischer A, De Villartay JP (1995): Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity. Science 268, 1347-1349.
    First description of homozygous and heterozygous mutations in CD95 in patients
  5. Friesen C, Herr I, Krammer PH, Debatin KM (1996): Involvement of the CD95 (APO-1/Fas) receptor/ ligand system in drug induced apoptosis in leukemia cell. Nat. Med. 2, 574-577.
    One of the first papers to describe the requirement for intact apoptosis signaling in cytotoxic drug induced apoptosis in leukemia cells
  6. Fulda S, Wick W, Weller M, Debatin KM (2002): Smac agonists sensitize for Apo2L/TRAIL- or anticancer drug-induced apoptosis and induce regression of malignant glioma in vivo. Nat. Med. 8, 808-15.
    One of the first papers to describe the synergy/requirement between inhibiting IAP proteins and sensitization for death receptor (TRAIL) induced apoptosis
  7. Meyer LH, Karawajew L, Schrappe E, Ludwig WD, Stahnke K, Debatin KM (2006): Cytochrome c related caspase activation determines treatment response and relapse in childhood B-precursor ALL. Blood 107, 4524-3.
    One of the first functional studies correlating intact apoptosis signaling in leukemia cells with treatment response
  8. Strauss G, Lindquist JA, Arhel N, Felder E, Karl S, Haas T, Fulda S, Walczak H, Kirchhoff F, Debatin KM (2009): CD95 co-stimulation blocks activation of naive T cells by inhibiting T cell receptor signaling. J. Exp. Med. 206, 1379-93.
    Identification of a novel role of the CD95 system in silencing T cell activation rather than inducing apoptosis in T cells
  9. Meyer LH, Eckhoff SM, Queudeville M, Kraus JM, Giordan M, Stursberg J, Zangrando A, Vendramini E, Moricke A, Zimmermann M, Schrauder A, Lahr G, Holzmann K, Schrappe M, Basso G, Stahnke K, Kestler HA, Te Kronnie G, Debatin KM (2011): Early relapse in ALL is identified by time to leukemia in NOD/SCID mice and is characterized by a gene signature involving survival pathways. Cancer Cell 19, 206-217.
    Identification of functional anti-apoptosis/survival signaling as a key prognostic factor in a large cohort of primary ALL cells in the NOD/SCID huALL model with translation of the results and the gene expression signature into clinical studies
  10. Münch V, Trentin L, Herzig J, Demir S, Seyfried F, Kraus JM, Kestler HA, Köhler R, Barth TFE, Te Kronnie G, Debatin KM, Meyer LH (2017): Central nervous system involvement in acute lymphoblastic leukemia is mediated by vascular endothelial growth factor. Blood 130, 643-654.
    First description of VEGF as a key regulator of CNS leukemia

For additional publications see ResearcherID.

Functions in Committees (Selection)
  • Since 2015: Vice President of Ulm University
  • Since 2013: Senate Commission on Key Questions in Clinical Research of the German Research Foundation (DFG)
  • 2013–2014: Board of Trustees of the German Cancer Aid
  • 2011–2017: Senate of the German Research Foundation (DFG)
  • 2009–2015: Steering Committee, Association of Medical Universities, Germany
Achievements and Awards (Selection)
  • 2011: German Cancer Aid Award
  • 2006: Descartes Prize (European Union)
  • 2005: Elected member: Heidelberg Academy of Sciences
  • 2002: German Cancer Award
  • 2001: Elected member: National Academy of Sciences (Leopoldina)