What topoisomerase intermediate do the authors conclude is stabilized by the drug?
How can this type of inhibition cause double-strand breaks, chromosomal rearrangements, and genomic instability?
How does topoisomerase’s role in DNA replication make this drug more lethal to cancer cells than to most somatic cells?
Look for other research studies that cite this one (very easy on Pubmed — ask me if you’re not sure how to do this), and comment briefly on how this research line of research has influenced science and society.