We have devised a barcoding strategy to recapitulate cancer evolution through the emergence of subclonal mutations of interest, whose effects can be monitored in a dynamic manner. This approach can be easily adapted for a variety of applications, including combined modeling of multiple mechanisms of drug resistance or repair of oncogenic driver mutations in addicted cancer cells.
Keywords: ALK; APC; CRISPR/Cas9; EGFR; TP53; genetic barcoding; non-small cell lung cancer; resistance; tumor heterogeneity.