Abstract
Genomic DNA barcoding has emerged as a sensitive and flexible tool to measure the fates of clonal subpopulations within a heterogeneous cancer cell population. Coupling cellular barcoding with single-cell transcriptomics permits the longitudinal analysis of molecular mechanisms with detailed clone-level resolution. Numerous recent studies have employed these tools to track clonal cell states in cancer progression and treatment response. With these new technologies comes the opportunity to examine longstanding questions about the origins and contributions of tumor cell heterogeneity and the roles of selection and phenotypic plasticity in disease progression and treatment.