GSE200926
Use of CRISPR/Cas9 with homology-directed repair to silence the human Topoisomerase IIa intron-19 5' splice site: Generation of etoposide resistance in human leukemia K562 cells
Results support the important role of both TOP2a/170 and TOP2a/90 as determinants of sensitivity/resistance to TOP2a-targeting agents. Overall design: CRISPR/Cas9 with homology-directed repair was utilized silencing of the exon 19/intron 19 5' splice site in parental K562 cells.