Bladder cancer exhibits high genomic heterogeneity, with an average of five mutations or more in the same tumor. Studying diverse higher-order genetic interactions that drive bladder cancer is difficult with current models of tumorigenesis, and it is limited by bulk sequencing which fails to directly discern clonality and resolve mutational co-occurrence patterns.
Dr. John Lee, of Fred Hutchinson Cancer Center, sought to better understand which combinations of mutations were critical by leveraging a mouse model, organoids, and gene-editing approaches. Using single-cell DNA sequencing, the Lee lab developed a system for investigating the functional impact of higher-order genetic interactions in cancer.
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