Tyrosinekinase inhibition facilitates cooperation of transcription factor SALL4 and ABC transporter A3 towards intrinsic CML cell drug resistance
Article first published online: 21 FEB 2013
© 2013 Blackwell Publishing Ltd
British Journal of Haematology
Volume 161, Issue 2, pages 204–213, April 2013
How to Cite
Hupfeld, T., Chapuy, B., Schrader, V., Beutler, M., Veltkamp, C., Koch, R., Cameron, S., Aung, T., Haase, D., LaRosee, P., Truemper, L. and Wulf, G. G. (2013), Tyrosinekinase inhibition facilitates cooperation of transcription factor SALL4 and ABC transporter A3 towards intrinsic CML cell drug resistance. British Journal of Haematology, 161: 204–213. doi: 10.1111/bjh.12246
- Issue published online: 3 APR 2013
- Article first published online: 21 FEB 2013
- Manuscript Accepted: 28 NOV 2012
- Manuscript Received: 7 OCT 2012
Fig S1. Enforced BCR-ABL expression is associated with ABCA3 expression, and ABCA3 transcripts arise from viable cells in from bcr-abl positive cell lines exposed to imatinib.
Fig S2. Silencing of SALL4 expression in BCR-ABL positive cell lines.
Fig S3. Silencing of SALL4 increases susceptibility of cell lines to cytotoxicity of tyrosine kinase inhibition.
Fig S4. Treatment with indomethacin reduces ABCA3 and SALL4 transcription.
Fig S5. Treatment with indomethacin sensitizes BCR-ABL positive cell lines to the cytotoxic effects of tyrosine kinase inhibition with imatinib, dasatinib and nilotinib.
Fig S6. Treatment with interferon gamma does not interfere with the cytotoxic effects of tyrosine kinase inhibition in BCR-ABL positive cell lines to.
Fig S7. Expression of ABCA3 in non-transformed hematopoietic cells, naive and under exposure to imatinib.
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