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ABSTRACT: Background
The encoding of cell intrinsic drug resistance states in breast cancer reflects the contributions of genomic and non-genomic variations and requires accurate estimation of clonal fitness from co-measurement of transcriptomic and genomic data. Somatic copy number (CN) variation is the dominant mutational mechanism leading to transcriptional variation and notably contributes to platinum chemotherapy resistance cell states. Here, we deploy time series measurements of triple negative breast cancer (TNBC) single-cell transcriptomes, along with co-measured single-cell CN fitness, identifying genomic and transcriptomic mechanisms in drug-associated transcriptional cell states.Results
We present scRNA-seq data (53,641 filtered cells) from serial passaging TNBC patient-de
SUBMITTER: Kabeer F
PROVIDER: S-EPMC11256464 | biostudies-literature | 2024 Jul
REPOSITORIES: biostudies-literature