Supplementary Materials

Supplementary Material for:

Tyrosine kinase inhibitor–induced CD70 expression mediates drug resistance in leukemia stem cells by activating Wnt signaling

Carsten Riether, Christian M. Schürch, Christoph Flury, Magdalena Hinterbrandner, Linda Drück, Anne-Laure Huguenin, Gabriela M. Baerlocher, Ramin Radpour, Adrian F. Ochsenbein*

*Corresponding author. E-mail: adrian.ochsenbein{at}

Published 29 July 2015, Sci. Transl. Med. 7, 298ra119 (2015)
DOI: 10.1126/scitranslmed.aab1740

This PDF file includes:

  • Materials and Methods
  • Fig. S1. TKI treatment induces CD70 expression on human BCR-ABL1+ leukemia cell lines.
  • Fig. S2. TKI treatment mediates CD70 induction via BCR-ABL1 inhibition.
  • Fig. S3. CD70 up-regulation is induced early after TKI treatment in KBM5r cells.
  • Fig. S4. Activation of Wnt signaling by lithium chloride or R-Spondin 1 restores TKI-mediated changes in gene expression.
  • Fig. S5. BCR-ABL1 and CD70/CD27 co-inhibition reduces the expansion of KBM5 and KBM5r CML cells in vitro.
  • Fig. S6. BCR-ABL1 and CD70/CD27 co-inhibition synergistically reduces cell growth and Wnt pathway activation in SD-1 cells.
  • Fig. S7. Combination treatment only marginally affects “healthy donor” BM stem/progenitor cells.
  • Fig. S8. Imatinib concentration was measured in the plasma of xenografted CML mice.
  • Fig. S9. CD70 and CD27 expression were determined on primary human CML cells.
  • Fig. S10. CD70 expression on murine LSCs and endogenous nonmalignant GFP LSKs was evaluated after imatinib treatment.
  • Fig. S11. TKI treatment induces CD70 expression on murine LSCs but not on leukemia progenitors or endogenous nonmalignant GFP LSKs.
  • Fig. S12. Combination therapy eradicates LSCs and promotes long-term survival of CML mice.
  • Table S1. Patient characteristics.
  • Table S2. Synergistic growth inhibition of SD-1 cells by targeting BCR-ABL1 and CD27 signaling.
  • Table S3. List of primers.

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