Somatic TP53 mutations characterize preleukemic stem cells in acute myeloid leukemia

Ridhima Lal, Karin Lind, Ellen Heitzer, Peter Ulz, Kristina Aubell, Karl Kashofer, Jan M. Middeke, Christian Thiede, Eduard Schulz, Angelika Rosenberger, Sybille Hofer, Birgit Feilhauer, Beate Rinner, Vendula Svendova, Michael G. Schimek, Frank G. Rücker, Gerald Hoefler, Konstanze Döhner, Armin Zebisch, Albert Wölfler and Heinz Sill

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  • TP53 mutation as an early leukemogenic event in acute lymphoblastic leukemia
    • Guranda Chitadze, Department of Hematology University Hospital Schleswig-Holstein

    G. Chitadze1,  M. Füllgrabe1, S. Neuburger2, H.-H. Oberg3, M. Kotrova1, M. Schwarz1,  D. Kabelitz3, N. Gökbuget4, M. Ritter2,  M. Brüggemann1

    1 Department of Hematology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany; 2 Department of Hematology and Internal Oncology, Sindelfingen Clinics, Sindelfingen, Germany; 3 Institute of Immunology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany; 4 Department of Medicine II, Goethe University Hospital,  Frankfurt, Germany


    To the Editor:

    A recent paper published in Blood by Lal et al.1 reported that somatic TP53 mutations characterize pre-leukemic stem cells (PreLSCs) in acute myeloid leukemia (AML) contributing to the disease development and therapeutic resistance.  

    We provide evidence that TP53 somatic mutations (e.g. TP53K132M) can characterize pre-leukemic cells also in acute lymphoblastic leukemia (ALL), and that they are able to generate differentiated progeny and persist in a non-leukemic compartment during remission.

    A 46-year-old female with B-cell precursor ALL (c-ALL with complex aberrant karyotype) responded well to induction/consolidation treatment protocol (GMALL registry NCT02872987) and achieved complet...

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    Conflict of Interest:
    None declared.