Supplementary Materials

The PDF file includes:

  • Fig. S1. 17p loss is a frequent genomic event in human breast cancer.
  • Fig. S2. Analysis of T cell markers in TNBC.
  • Fig. S3. Analysis of immune-related pathways for 17ploss versus 17pintact TNBCs.
  • Fig. S4. Analysis of HER2 status in TNBC samples.
  • Fig. S5. HER2 and 17p status of TNBC cell lines determines their sensitivity to the treatment with α-amanitin and T-Ama in vitro and in vivo.
  • Fig. S6. Generation of HER2-low/17ploss isogenic cell lines from parental HS578T cells.
  • Fig. S7. Cells lacking HER2 expression are insensitive to T-Ama.
  • Fig. S8. Validation of HER2 expression levels in tumor sections.
  • Fig. S9. T-Ama treatment of mice resulted in no overt toxicity.
  • Fig. S10. Liver function after treatment with anti–digoxigenin–α-amanitin conjugates in female cynomolgus monkeys.
  • Fig. S11. α-Amanitin induces apoptosis in breast cancer cells in vitro.
  • Fig. S12. α-Amanitin induces ICD in breast cancer cells in vitro.
  • Fig. S13. α-Amanitin–induced cell death of tumor cells stimulates the maturation of BMDCs.
  • Fig. S14. Generation of isogenic EO771 cell line with heterozygous 11B loss.
  • Fig. S15. T-Ama treatment increases T cell infiltration and expression of cytotoxic markers in subcutaneous murine breast cancer tumors.
  • Fig. S16. T-Ama treatment enhances T cell infiltration into mammary gland–implanted tumors.
  • Fig. S17. T-Ama treatment has no overt toxicity on the mammary glands of HER2 transgenic mice.
  • Table S1. Antibody panel for total immune profiling analysis in CyTOF.
  • Table S2. Antibody panel for T cell analysis in CyTOF.

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Raw data for main figures and supplementary figures.