Extended Data Fig. 10: Pharmacological inhibition of PGE2 and type I IFN modulators resensitize cross-resistant tumors to immunotherapy.
From: Cancer cells impair monocyte-mediated T cell stimulation to evade immunity
a, Relative frequency of each cell type across conditions (scRNA-seq). b, Scoring of the Duong et al. inflammatory signature37 in RTT COX2i-treated tumors. c, Heatmap of scaled gene expression (scRNA-seq) in YUMM1.7 OVA RTT vehicle-treated tumors (CTRL) and RTT celecoxib (COX2i)-treated tumors (n = 3 tumors were pooled/group). d, Response of YUMM1.7OVA RTT tumors to vehicle + adoptive T cell transfer (ACT) (n = 7 mice), celecoxib (n = 4 mice), celecoxib + ACT (n = 6 mice) and etoricoxib ± ACT (n = 7 mice/group). Red arrow and box indicate COX2i treatment stop. e, UMAP of scRNA-seq of CD45+ cells from YUMM1.7OVA RTT mice treated with vehicle or COX2i + 5-AZA isolated 72 h post-ACT (n = 3 tumors pooled/group). f, Relative frequency of each cell type across conditions in e (scRNA-seq). g, Scoring of the Duong et al. inflammatory signature37 in COX2i + 5-AZA treated tumors. h, Response of YUMM1.7OVA RTT tumors to 5-azacytidine (5-AZA) (n = 4 mice), 5-AZA + ACT (n = 7 mice), vehicle+ACT (n = 8 mice), Flt3L+ACT (n = 7 mice), COX2i+ACT (n = 9 mice), COX2i + 5-AZA + ACT (n = 7 mice) and COX2i+Flt3L+ACT (n = 8 mice). i, Representative image of IF staining of vehicle-treated and COX2i+Flt3L RTT YUMM1.7OVA tumors 96 h post-ACT (n = 2 tumors per condition). Scale bar = 1000 µm, zoom-in = 50 µm. Black arrows indicates day of ACT.
