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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Cancer Discov. 2017 Jan 20;7(3):302–321. doi: 10.1158/2159-8290.CD-16-0653

Figure 1.

Figure 1

Response to MEK inhibition in TNBC patient tumors from window-of-opportunity clinical trial. (A) Transcriptional response to trametinib in TNBC patient tumors in pre-treatment needle core biopsies (NCBs) and in corresponding surgical resections following 7 day trametinib treatment. Total number of expressed genes are indicated in black; percentage of transcripts induced (red) or suppressed (green) > 2 fold after trametinib treatment are indicated. (B) Tyrosine kinome transcriptional response (> 1.5 fold) to trametinib treatment in BL;BL patient tumors (blue) or CL;CL patient tumor (red). (C) Differential Expression-Seq2 (DESeq2) analysis comparing pre-trametinib and post-trametinib BL;BL tumors. Shown are differentially expressed kinases using 0.05 FDR for significance. Pt. 4 was excluded from the DESeq2 analysis because of high immune kinase expression but presented in the heat map for comparison. CL;CL tumor 6 is presented in the heat map for comparison to the BL;BL tumor response. (D) Adaptive response RTK protein upregulation in BL;BL patient tumors. (E) Scatterplot of RSEM transcript abundance values vs. MIB/MS TK MIB binding as a ratio of trametinib-treated surgical resection:pre-treatment NCB in BL;BL Pt. 5 (blue) and CL;CL Pt. 6 (red). Non-TKs are indicated with black circles. Arrows highlight decreased MEK1/2 MIB binding following trametinib.

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