Fig. 1: Residual tumours, but not adjacent normal tissues, are enriched with RASAL2.
From: CREB1-BCL2 drives mitochondrial resilience in RAS GAP-dependent breast cancer chemoresistance

A UMAP plots of epithelial cells from primary TNBC tumours showing correlation between CytoTRACE score (1—least differentiation, 0 – most differentiation) and RASAL2 expression. B Violin plots of RASAL2 expression and residual tumour signature expression in the four clusters of epithelial cells identified in the TNBC tumours in (A). Cluster 1 expressions are significantly higher compared to all other clusters. Data are represented as mean ± SEM. P value by one-way ANOVA. C Heatmap of RASAL2 expression in pre- and post-treatment breast cancer patients [19]. Fold change (FC) was determined relative to pre-treatment expression level. P value by paired T-test. D Dot plots of RASAL2 expression in pre- versus post-treatment TNBC/BRCA-mutant breast cancer patients [20]. Probes that recognise RASAL2 variant 2 (ILMN_1813701 and ILMN_1673455) show significant increase following treatment. Data are represented as mean ± SEM. P value by two-tailed T-test. E Immunohistochemistry of fixed post-treatment TNBC patient breast specimens. RASAL2 (brown stain) was enriched in the tumour compartment versus adjacent normal epithelia. Data are represented as mean ± SEM. P value by two-tailed T-test. Scale bar, 20 µm. F Immunoblotting of fresh post-treatment TNBC patient specimens. RASAL2 was enriched in the tumour (T) versus adjacent normal (N) tissues in TNBC patients. LE long exposure.