Single-cell lineage analysis reveals genetic and epigenetic interplay in glioblastoma drug resistance.

ABSTRACT:

Background

Tumors can evolve and adapt to therapeutic pressure by acquiring genetic and epigenetic alterations that may be transient or stable. A precise understanding of how such events contribute to intratumoral heterogeneity, dynamic subpopulations, and overall tumor fitness will require experimental approaches to prospectively label, track, and characterize resistant or otherwise adaptive populations at the single-cell level. In glioblastoma, poor efficacy of receptor tyrosine kinase (RTK) therapies has been alternatively ascribed to genetic heterogeneity or to epigenetic transitions that circumvent signaling blockade.

Results

We combine cell lineage barcoding and single-cell transcriptomics to trace the emergence of drug resistance in stem-like glioblastoma cells treate

SUBMITTER: Eyler CE 

PROVIDER: S-EPMC7364565 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature