Acute myeloid leukemia (AML) with activated Fms-like tyrosine kinase receptor III (FLT3) causes significant mortality secondary to relapsed/refractory (R/R) disease. Drug resistance limits the duration of response of FLT3 inhibitors (FLT3i). Genetic evolution leading to R/R disease is incompletely understood, and leukemia’s heterogeneity is incompletely described, even with next-generation sequencing (NGS). A deeper understanding of cellular heterogeneity is essential because intratumoral heterogeneity is ubiquitous, has prognostic relevance, affects response to therapy, and drives therapeutic resistance. We characterized, via single-cell sequencing (SCS), the genetic evolution of R/R AML on the FLT3i quizartinib.
Peretz, C.A.C, McGary, L.H.F, Kumar, T., Jackson, H., Jacob, J., Durruthy-Durruthy, R., Levis, M.J., Perl, A., Huang, B.J., Smith, C.C.