Supplementary Fig. 9: Residual triple-negative breast tumor model of acquired resistance to Capecitabine.
From: High-throughput single-cell ChIP-seq identifies heterogeneity of chromatin states in breast cancer
(a) n = 6 mice with HBCx-95 derivatives were treated with Capecitabine for 6 weeks. Graphs represent relative tumor volumes (RTV, mm3) with time. Mice with recurrent tumors were treated for a second round of Capecitabine when PDX reached a volume of over 200 mm3 (mice #35, #40 & #33). Mouse #40 did not respond to Capecitabine and the PDX specimen was extracted at 1080 mm3 and tagged as HBCx-95-CapaR. Samples studied in manuscript are indicated with a dashed rectangle. (b) Histograms of the distribution of scChIPseq raw and unique sequencing reads per cell in untreated HBCx-95 and Capecitabine-resistant HBCx-95-CapaR PDX. (c) Scatter plot displaying the log2 enrichments in cumulative single-cell versus bulk H3K27me3 ChIP-seq data, calculated based on the counts per million mapped reads in 50 kb genomic bins (n = 54,650 genomic bins). Pearson’s correlation score and P value are computed genome-wide. (d) Distribution of the log2 enrichments in 50 kb genomic bins for cumulative single-cell and bulk H3K27me3 ChIP-seq data. Amplitude between maximum and minimum log2 enrichments are indicated on the top right for each ChIP-seq method (either bulk or single-cell).
