Reversing myeloid-derived suppressor cells mediated immunosuppression via p38a inhibition enhances immunotherapy efficacy
By combining the tumor immunological phenotype (TIP) gene signature and high throughput sequencing based high throughput screening (HTS2), we identified that ponatinib significantly inhibits the expression of “cold” tumor associated chemokines CXCL1 and CXCL2 in cancer cells. To investigate how ponatinib regulates the expression of “cold”-tumor related genes CXCL1 and CXCL2, we conducted RNA-seq study to examine transcriptome-wide effects of ponatinib with both MDA-MB-231 cells and 4T1 cells. Overall design: Comparative transcriptome analysis of RNA-seq data for TNBC cells treated with ponatinib or DMSO.