Supplementary Materials

Supplementary Material for:

Integration of Hedgehog and mutant FLT3 signaling in myeloid leukemia

Yiting Lim, Lukasz Gondek, Li Li, Qiuju Wang, Hayley Ma, Emily Chang, David L. Huso, Sarah Foerster, Luigi Marchionni, Karen McGovern, David Neil Watkins, Craig D. Peacock, Mark Levis, Bruce Douglas Smith, Akil A. Merchant, Donald Small, William Matsui*

*Corresponding author. E-mail: matsuwi{at}jhmi.edu

Published 10 June 2015, Sci. Transl. Med. 7, 291ra96 (2015)
DOI: 10.1126/scitranslmed.aaa5731

This PDF file includes:

  • Fig. S1. GLI2 is expressed in FLT3-ITD AML clinical specimens.
  • Fig. S2. Flt3/ITD-SmoM2 transgenic mice express Hh pathway genes and develop clinically relevant AML.
  • Fig. S3. Specific bone marrow hematopoietic stem cell and myeloid progenitor compartments are maintained in Flt3/ITD-SmoM2 mice.
  • Fig. S4. Leukemia formation in Flt3/ITD-SmoM2 mice is cell-intrinsic.
  • Fig. S5. GSEA reveals increased STAT5 signaling in Flt3/ITD and antiapoptotic features in Flt3/ITD-SmoM2 mice.
  • Fig. S6. The combination of sorafenib and IPI-926 limits the growth of FLT3-ITD AML.
  • Fig. S7. Hh signaling affects FLT3-ITD at the level of STAT5.
  • Fig. S8. IPI-926 inhibits the expression of Hh target genes in Flt3/ITD-SmoM2 bone marrow cells.
  • Table S1. Leukemic organ infiltration.
  • Table S2. PCR primers.
  • Other Supplementary Material for

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Other Supplementary Material for this manuscript includes the following:

  • Table S3. Original data (provided as a separate Excel file).

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