Fig. 7: MYC and SMAD4 play opposing roles in pancreatic tumor maintenance.
From: KRAS drives immune evasion in a genetic model of pancreatic cancer
a, b Heatmaps from scRNA-seq showing differentially expressed TGF-beta/SMAD and MYC pathway genes in KRAS intact, KRAS KO, and BRAF/MYC reconstituted KPC tumors. c, d The mean latency (c) and efficiency (d) of orthotopic tumor development in wild-type mice by KRAS KO and KRAS/SMAD4 KO KPC cells (n = 5 for each genotype) transduced with the indicated genes. Data are presented as mean ± SD, two-tailed t-test. e, f Histology and quantification of IHC staining of tumors (n = 5 for each genotype). Data are expressed as mean ± SD. Significance was determined using two-tailed test at the 0.05 confidence interval. Scale bar 200 μM. g Conceptual schematic of phenotypic changes in PDAC tumors. BRAF and MYC are key mediators of KRAS-induced immune evasion. Loss of SMAD4 enhances KRAS-independent tumor growth.
