Supplementary Materials

Supplementary Material for:

Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence

Justin M. Balko,* Luis J. Schwarz, Na Luo, Mónica V. Estrada, Jennifer M. Giltnane, Daniel Dávila-González, Kai Wang, Violeta Sánchez, Phillip T. Dean, Susan E. Combs, Donna Hicks, Joseph A. Pinto, Melissa D. Landis, Franco D. Doimi, Roman Yelensky, Vincent A. Miller, Phillip J. Stephens, David L. Rimm, Henry Gómez, Jenny C. Chang, Melinda E. Sanders, Rebecca S. Cook, Carlos L. Arteaga*

*Corresponding author. E-mail: carlos.arteaga{at} (C.L.A.); justin.balko{at} (J.M.B.)

Published 13 April 2016, Sci. Transl. Med. 8, 334ra53 (2016)
DOI: 10.1126/scitranslmed.aad3001

This PDF file includes:

  • Fig. S1. Focal and nonfocal amplifications at 9p24/JAK2 exist in ER-negative breast cancer.
  • Fig. S2. JAK2 copy number is associated with JAK2 gene expression.
  • Fig. S3. Ruxolitinib has low impact on gene expression in vitro.
  • Fig. S4. Ruxolitinib does not reduce cell viability or enhance chemosensitivity in vitro.
  • Fig. S5. JAK2 knockdown reduces mammosphere potential in HCC-38 and MDA-436 cells.
  • Fig. S6. Pharmacological inhibition of JAK2 reduces mammosphere formation after chemotherapy selection in vitro.
  • Fig. S7. JAK2 inhibition overcomes taxane resistance in PDXs with JAK2GAIN.

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