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A unifying framework disentangles genetic, epigenetic, and stochastic sources of drug-response variability in an in vitro model of tumor heterogeneity
[article]
2020
bioRxiv
pre-print
Tumor heterogeneity is a primary cause of treatment failure and acquired resistance in cancer patients. Even in cancers driven by a single mutated oncogene, variability of targeted therapy response is observed. Additional genetic mutations can only partially explain this variability, leading to consideration of non-genetic factors, such as "stem-like" and "mesenchymal" phenotypic states, as critical contributors to tumor relapse and resistance. Here, we show that both genetic and non-genetic
doi:10.1101/2020.06.05.136119
fatcat:otedawbpvnaz5jybjvxmzgcfsi