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. 2022 Sep 26;28(20):4494–4508. doi: 10.1158/1078-0432.CCR-22-0543

Figure 2.

Figure 2. Immune context of immunologically cold chemotherapy-resistant ER+HER2– and TNBC breast cancers. A, Representative multiplexed IHC images showing staining of key lineage markers and immune-checkpoint expression in tissue sections. B, Bar charts showing immune composition of ER+HER2– (n = 16, blue) and TNBC (n = 15, red) residual disease samples. Statistical analysis to compare immune composition between subtypes was performed using the two-stage Mann–Whitney test. C, Log2 FC in immune cell types in residual disease samples compared with pretreatment samples in (i) ER+HER2– disease (n = 10 matched-paired samples) and (ii) TNBC (n = 10 matched paired samples; Wilcoxon matched-pairs signed rank test; *, P ≤ 0.05; **, P ≤ 0.01). D(i–ii), Percentage of tumoral and stromal PD-L1 expression within the TIME of TNBC RCB II/III disease. D(iii–iv), Percentage of PD-1 expression on immune cells found within the invasive tumor (iii) and tumor stroma (iv) in TNBC RCB II/III disease (Mann–Whitney test; *, P ≤ 0.05; **, P ≤ 0.01; ****, P ≤ 0.0001). E, Representative image of a selected ROI for digital spatial profiling based on CD45 staining. Per patient 12 ROIs were selected in TIL-rich areas where possible. Areas of 600 μm in diameter were placed. F and G, Quantification of protein expression of immune cell lineage markers and immune checkpoints in selected ROIs from ER+HER2– and TNBC residual disease samples. H, Heatmap showing differential protein expression of significantly upregulated or downregulated immune-checkpoint markers within TNBC RCB II/III tumors compared with pre-NAC baseline samples. Only those immune-checkpoint receptors where they were significant in at least 2 of 3 patients with FC in the same direction are indicated (P < 0.05; see also Supplementary Table S3).

Immune context of immunologically cold chemotherapy-resistant ER+HER2– and TNBC breast cancers. A, Representative multiplexed IHC images showing staining of key lineage markers and immune-checkpoint expression in tissue sections. B, Bar charts showing immune composition of ER+HER2– (n = 16, blue) and TNBC (n = 15, red) residual disease samples. Statistical analysis to compare immune composition between subtypes was performed using the two-stage Mann–Whitney test. C, Log2 FC in immune cell types in residual disease samples compared with pretreatment samples in (i) ER+HER2– disease (n = 10 matched-paired samples) and (ii) TNBC (n = 10 matched paired samples; Wilcoxon matched-pairs signed rank test; *, P ≤ 0.05; **, P ≤ 0.01). D (i–ii), Percentage of tumoral and stromal PD-L1 expression within the TIME of TNBC RCB II/III disease. D (iii–iv), Percentage of PD-1 expression on immune cells found within the invasive tumor (iii) and tumor stroma (iv) in TNBC RCB II/III disease (Mann–Whitney test; *, P ≤ 0.05; **, P ≤ 0.01; ****, P ≤ 0.0001). E, Representative image of a selected ROI for digital spatial profiling based on CD45 staining. Per patient 12 ROIs were selected in TIL-rich areas where possible. Areas of 600 μm in diameter were placed. F and G, Quantification of protein expression of immune cell lineage markers and immune checkpoints in selected ROIs from ER+HER2– and TNBC residual disease samples. H, Heatmap showing differential protein expression of significantly upregulated or downregulated immune-checkpoint markers within TNBC RCB II/III tumors compared with pre-NAC baseline samples. Only those immune-checkpoint receptors where they were significant in at least 2 of 3 patients with FC in the same direction are indicated (P < 0.05; see also Supplementary Table S3).