Acute myeloid leukemia (AML) is a lethal malignancy because patients who initially respond to chemotherapy eventually relapse with treatment refractory disease. Relapse is caused by leukemia stem cells (LSCs) that reestablish the disease through self-renewal. Self-renewal is the ability of a stem cell to produce copies of itself and give rise to progeny cells. Therefore, therapeutic strategies eradicating LSCs are essential to prevent relapse and achieve long-term remission in AML. AML is a heterogeneous disease both at phenotypic and genotypic levels, and this heterogeneity extends to LSCs. Classical studies in AML have aimed at characterization of the bulk tumor population, thereby masking cellular heterogeneity. Single-cell approaches provide a novel opportunity to elucidate molecular mechanisms in heterogeneous diseases such as AML. In recent years, major advancements in single-cell measurement systems have revolutionized our understanding of the pathophysiology of AML and enabled the characterization of LSCs. Identifying the molecular mechanisms critical to AML LSCs will aid in the development of targeted therapeutic strategies to combat this deadly disease.
Bibliographical noteFunding Information:
ZS was supported by American Cancer Society Mentored Research Scholar grant, Frederick A. DeLuca Foundation, ( MRSG-16-195-01-DDC ); Clinical and Translational Science Institute at the University of Minnesota KL2 Career Development Award NIH/NCATS ULI RR033183 and KL2 RR0333182; the division of Hematology, Oncology, and Transplantation, Department of Medicine, University of Minnesota; University of Minnesota Department of Medicine Women's Early Research Career Award, Masonic Cancer Center Pilot grants, and an American Cancer Society Institutional Research grant.