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AG Oncogenic Signaling Laboratory

  • Arbeitsgruppenleiter:in: 

    PD Dr. med. Thomas Kindler (UCT Mainz, Department of Hematology, Medical Oncology & Pneumology)
  • Forschungsschwerpunkte:

    Our group is interested to understand oncogenic signaling and its effect on the regulation of gene transcription, epigenetic modulation and genetic stability. During tumorigenesis, acquired genetic alterations cause oncogenic stress, aberrant DNA damage repair and a block in differentiation. A detailed understanding of the interaction of disturbed and rewired signaling pathways will help us to uncover mechanisms of specific vulnerabilities in cancer cells. The overall aim of the group is to develop novel therapeutic strategies and its transfer into the clinic.

    Current research topics:
    -
    Exploring the role of mutant KRAS, the most common cancer oncogene, in DNA damage repair
    - Analysis of PARP-inhibitors as a therapeutic option in lung cancer and leukemia and it´s effect on defined immune cell populations
    - Impact of the transcription factor STAT5 on epigenetic modulation and RNA processing in AML and solid tumours

    We take advantage of well-established experimental approaches and tumor models including primary patient samples and in vivo models. The lab is closely embedded in the scientific landscape of the UCT and partner of several (inter)national collaborations.
  • Fünf wichtigste Publikationen:

    Sasca D, Szybinski J, Schüler A, Shah V, Heidelberger J, Haehnel PS, Dolnik A, Kriege O, Fehr EM, Gebhardt WH, Reid G, Scholl C, Theobald M, Bullinger L, Beli P, Kindler T. NCAM1 (CD56) promotes leukemogenesis and confers drug resistance in AML. Blood. 2019; 133(21):2305-19.

    Sasca D, Hähnel PS, Szybinski J, Khawaja K, Kriege O, Pante SV, Bullinger L, Strand S, Strand D, Theobald M, Kindler T. SIRT1 prevents genotoxic stress-induced p53 activation in acute myeloid leukemia. Blood. 2014;124(1):121-33.

    Hähnel PS, Enders B, Sasca D, Roos WP, Kaina B, Bullinger L, Theobald M, Kindler T. Targeting components of the alternative NHEJ pathway sensitizes KRAS mutant leukemic cells to chemotherapy. Blood. 2014;123(15):2355-66.

    Tam WF, Hähnel P, Schüler A, Lee BH, Okabe R, Zhu N, Pante S, Raffel G, Mercher T, Wernig G, Bockamp E, Kreft A, Robinson GW, Hennighausen L, Gilliland DG, Kindler T. STAT5 is crucial for the maintenance of leukemic stem cells in MOZ-TIF2 induced acute myeloid leukemogenesis. Cancer Research. 2013;73(1):373-84.

 

 

 

 


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Ansprechpartnerin:

 

Sabine Tensing

Programmkoordination
MAInz-DOC-Promotionskolleg

Tel +49 6131 17-7632
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