Data File S3 from Dose and Schedule Determine Distinct Molecular Mechanisms Underlying the Efficacy of the p53–MDM2 Inhibitor HDM201

Insertional results from Arf-/- PB in vivo resistance screens. A and C, Tables listing all sequenced samples with their model number (i.e. X25272), the transplanted fragment number (i.e. P0M1-P1M5-P2M19, P for passage, and M for Mouse), tumor status (DR=drug resistant, or veh=vehicle treated) and treatment schedule (A) QD for daily or (C) 2QW for biweekly. Total number of reads and tumor pathology are labeled for each sample. Insertional landscapes are displayed on the right part of the table where the averaged normalized diversity sequencing counts are indicated for each Common insertion site gene (gCIS) and each tumor. B and D, List of the genes found differentially enriched for PB insertions in HDM201 resistant tumors compared to untreated tumors (B) continuous daily treatment or (D) biweekly intermittent treatment. The data in D were extracted from previous report (28) for intermittent 100 mg/kg biweekly dosing schedule, and reanalyzed with only 6 tumor models used out of 16 in previous report. Fold change, p-value and FDR were calculated for each gene in comparative analyses of untreated tumor samples vs. resistant tumor samples. PercentSample indicated the percentage of resistant tumors with insertion in that gene. The predicted function GOF (gain of function), LOF (loss of function) or uncertain is also indicated.