Pre-existing stem cell heterogeneity dictates clonal responses to the acquisition of leukemic driver mutations.

Abstract excerpt

Cancer cells display wide phenotypic variation even across patients with the same mutations. Differences in the cell of origin provide a potential explanation, but traditional assays lack the resolution to distinguish clonally heterogeneous subsets of stem and progenitor cells. To address this challenge, we developed simultaneous tracking of recombinase activation and clonal kinetics (STRACK), a method to trace...

Topics

• Animals
• Mutation
• Nucleophosmin
• Mice
• Humans
• DNA Methyltransferase 3A
• Clone Cells