Supplementary Materials

Supplementary Material for:

PI3K inhibition results in enhanced estrogen receptor function and dependence in hormone receptor–positive breast cancer

Ana Bosch, Zhiqiang Li, Anna Bergamaschi, Haley Ellis, Eneda Toska, Aleix Prat, Jessica J. Tao, Daniel E. Spratt, Nerissa T. Viola-Villegas, Pau Castel, Gerard Minuesa, Natasha Morse, Jordi Rodón, Yasir Ibrahim, Javier Cortes, Jose Perez-Garcia, Patricia Galvan, Judit Grueso, Marta Guzman, John A. Katzenellenbogen, Michael Kharas, Jason S. Lewis, Maura Dickler, Violeta Serra, Neal Rosen, Sarat Chandarlapaty,* Maurizio Scaltriti,* José Baselga*

*Corresponding author. E-mail: chandars{at} (S.C.); scaltrim{at} (M.S.); baselgaj{at} (J.B.)

Published 15 April 2015, Sci. Transl. Med. 7, 283ra51 (2015)
DOI: 10.1126/scitranslmed.aaa4442

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Western blot of MCF7 and T47D cells treated in vitro with BYL719 for a series of time points.
  • Fig. S2. T47D transcriptional profile upon p110α inhibition.
  • Fig. S3. GSEA for T47D microarray expression data set.
  • Fig. S4. Western blot of CAMA1 cells treated with BYL719 or MK2206 for 48 hours.
  • Fig. S5. CAMA1 transcriptional profile after AKT inhibition.
  • Fig. S6. ER target genes induced by AKT inhibition in ER-positive/PTENmut/null breast cancer cells.
  • Fig. S7. ESR1 expression induced by PI3Kα inhibition in ER-positive/PIK3CAmut breast cancer cells.
  • Fig. S8. ESR1 transcription increased by PI3Kα inhibition.
  • Fig. S9. Induction of ESR1 and its target genes by different PI3K inhibitors.
  • Fig. S10. Comparison of induction of ESR1 and its target genes between BYL719 and the mTORC1 allosteric inhibitor rapamycin.
  • Fig. S11. Decreased expression of ER target genes after anti-ER therapy, with no effect on ESR1 mRNA.
  • Fig. S12. Up-regulation of ER target genes reversed by combining BYL719 with anti-ER treatment.
  • Fig. S13. Better tumor control in vivo after combining BYL719 with fulvestrant.
  • Fig. S14. Analysis of the effect of PI3Kα inhibition alone or with anti-ER therapy on the cell cycle.
  • Table S1. GSEA to assess ER-dependent signatures enriched in MCF7 cells treated with BYL719.
  • Table S2. GSEA to assess ER-dependent signatures enriched in CAMA1 cells treated with MK2206.
  • Table S3. Clinical and pathologic features corresponding to paired pretreatment and BYL719-treated tumor samples.
  • References (4345)

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Other Supplementary Material for this manuscript includes the following:

  • Table S4. Raw data (provided as an Excel file).

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