Supplementary Materials

The PDF file includes:

  • Fig. S1. Validation of Gr-1 depletion through quantification of CD11b+Ly6G+ neutrophils.
  • Fig. S2. Quantification of intravital imaging demonstrated decreased tumor NF-κB transcriptional activation and increased host MPO activity in MPO+/+ compared to MPO−/− animals.
  • Fig. S3. Confocal images of B16F10 NF-κB-FLuc cells that are distant from or in close proximity to MPO+/+ MDCs.
  • Fig. S4. Histology of end point B16F10 tumors from MPO+/+ and MPO−/− animals and MPO activity and expression in B16F10 melanoma cells.
  • Fig. S5. Plasma cytokine concentration changes in MPO+/+, MPO−/−, and 4-ABAH–treated MPO+/+ animals observed only at early tumor growth time points.
  • Fig. S6. Increased basal NF-κB activation in B16F10 NF-κB-FLuc monoclones was associated with enhanced in vitro growth but not in vivo tumor growth.
  • Fig. S7. B16F10 reporter cells in close proximity to MPO+/+ MDCs demonstrated decreased NF-κB transcriptional activation compared to tumor cells distant from MPO+/+ MDCs.
  • Fig. S8. Bone marrow–derived MDCs from MPO+/+ animals, but not those from MPO−/− animals, inhibited melanoma cell IκB degradation.
  • Fig. S9. HOCl inhibited basal NF-κB transcriptional activation in B16F10 reporter tumor cells.
  • Fig. S10. HOCl inhibited TNFα-stimulated NF-κB signaling in live cells.
  • Fig. S11. Different genes were affected by HOCl in melanoma cells compared to T cells.
  • Fig. S12. HOCl changed the cytokines secreted by B16F10 melanoma cells.
  • Fig. S13. HOCl did not affect the cytokines secreted by CD8+ T cells isolated from the spleen.

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