Fig. 2

Low FOXO activity corresponds with a poor nCRT responder phenotype in EAC patient samples. A Activity of six key signal transduction pathways was measured in the resectable disease cohort (i) and compared to clinicopathological outcome data. Shown pathways from left to right: androgen receptor (AR), estrogen receptor (ER), Phosphatidylinositol 3-Kinase/Forkhead Box O (FOXO), Hedgehog (HH), Transforming growth factor receptor Beta (TGF-β) and Wnt pathway. Pre-treatment biopsy pathway activity scores were subtracted from matched post-nCRT resections (N = 56), yielding a delta activity score. Unique samples that passed QC were excluded from analysis. Two-sided Wilcoxon signed-rank statistical tests were performed between Mandard low (1–3, N = 40) and Mandard high (4–5, N = 16) patients per pathway. B Pathway activity scores of pre-treatment EAC biopsies in the recurrent disease cohort with known Mandard score (N = 77). Both matched and unique samples were included for analysis. Wilcoxon statistical tests compare Mandard low (1–3, N = 61) and Mandard high (4–5, N = 16) patients per pathway. C Pathway activity scores of non-treated EAC resection tissue from both the resected and recurrent disease cohort (N = 37 + 47 = 84) and adjacent healthy esophageal tissue (N = 20). D Pathway signal transduction activity was measured in the recurrent disease cohort (ii). Pathway activity scores of all resected specimens (N = 150) and recurrences (N = 20) that passed QC are shown. p-values are indicated in the figures. Boxplots represent median with interquartile range