Cancer Susceptibility to Stapled Oncolytic Peptides is Dictated by Membrane Cholesterol and Inflammatory Signaling

Whole-exome sequencing (WES) was performed to characterize genomic alterations associated with induced drug resistance in OCI-AML3 cells. Genomic DNA from parental and independently derived resistant OCI-AML3 clones was extracted and subjected to exome capture followed by paired-end next-generation sequencing. Reads were aligned to the human reference genome (hg38), and standard best-practice pipelines were used for quality control, duplicate marking, base recalibration, and variant calling. Somatic single-nucleotide variants and small insertions/deletions were identified and compared between parental and resistant lines to define clonal signatures of resistance. Copy-number alterations were inferred from exome read depth and allele frequency profiles to determine genome-wide copy-number status and clonal evolution associated with resistance.