Fifty percent (50%) of patients with acute myeloid leukemia (AML) relapse and develop a more virulent form of the disease. To better understand AML and the cancer hematological ecosystem, it is necessary to discern clonal architecture and the dynamics of competing clones, which provide valuable insight into therapy response. It takes three or more mutations for leukemia to form. This can occur in the same cell or within the tumor microenvironment, but how do you discern this information with bulk sequencing? Dr. Jerry Radich, of Stanford Medical Center, and Dr. Koichi Takahashi, of MD Anderson, share their research on how they identified mutations within rare subclones using single-cell analysis for precision over bulk sequencing.
