Figure 5 from p53R172H and p53R245W Hotspot Mutations Drive Distinct Transcriptomes in Mouse Mammary Tumors Through a Convergent Transcriptional Mediator

Transcriptomic meta-analysis of human breast tumors with TP53R175H and TP53R248W/Q mutations recapitulates NR5A2 as a co-regulator. A, Supervised clustering of human breast tumors from METABRIC dataset harboring a TP53R175H mutation compared with human breast tumors with a homozygous deletion of TP53. B, Pie chart representing significantly DEGs for TP53R175H breast tumors compared with TP53-null breast tumors (limma), significance criteria were FDR <5% and fold change >1.5. C, Supervised clustering of human breast tumors from METABRIC dataset harboring a TP53R248Q or TP53R248W mutation compared with human breast tumors with a homozygous deletion of TP53. D, Pie chart representing DEGs for TP53R248Q/W breast tumors compared with TP53-null breast tumors (limma), significance criteria were FDR <5% and fold change >1.5. E, NR5A2 binding motif sequences identified by MEME from JASPAR database. F, Oncoprint analysis in cBioportal to assess co-occurrence of TP53 mutations with NR5A2 amplifications. G, Prevalence of co-occurrence of TP53 missense mutations with NR5A2 amplification across human molecular breast cancer subtypes: luminal A (38%), luminal B (26%), HER2-enriched (15%), and TNBC (21%).