Fig. 4

Candidate molecular pathways stratify patients based on response to carboplatin–taxane in an independent cohort. a Validation strategy, as follows: first, employment of molecular transcriptomic and epigenomic profiling of patients; second, predicting patients’ risk of developing chemoresistance; and finally, informed clinical decision making based on patients personalized risks. b t-SNE clustering of lung adenocarcinoma patients treated with carboplatin–taxane (e.g., paclitaxel) from the Tang et al. validation cohort (n = 39 biologically independent patient samples), based on activity levels of seven candidate pathways. Among two groups green group (n = 21 biologically independent patient samples) corresponds to patients with low composite activity levels of candidate pathways and orange group (n = 18 biologically independent patient samples) corresponds to patients with high composite activity levels of candidate pathways. c Kaplan–Meier survival analysis to estimate difference in response to carboplatin–taxane (e.g., paclitaxel) between two patient groups is identified in b. Log-rank p-value and number of patients in each group are indicated. d Two random models indicate non-random predictive ability of our model in the Tang et al. validation cohort: random model 1 (steel-blue) is defined based on to seven pathways selected at random, and random model 2 (goldenrod) is defined based on to equally sized patient groups selected at random