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Related Experiment Video

Updated: Jul 18, 2026

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up

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Leukemia: stem cells, maturation arrest, and differentiation therapy.

¹Wadsworth Center and Ordway Research Institute, New York State Department of Health, Albany, NY 12201, USA. ssell@wadsworth.org

Stem Cell Reviews

|December 5, 2006

Summary

Targeted therapies inhibiting specific genetic mutations in myeloid leukemias allow cancer cells to differentiate and die. Combinations of inhibitors offer promise for more effective, permanent treatments.

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Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia

Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia

Published on: March 5, 2018

Area of Science:

Oncology
Hematology
Molecular Biology

Background:

Leukemia involves impaired myeloid cell differentiation, leading to uncontrolled proliferation.
Genetic mutations in leukemia cause maturation arrest, preventing normal cell death.
Specific genetic lesions drive leukemic cell growth and survival.

Purpose of the Study:

To explore targeted therapies for human myeloid leukemias.
To investigate how inhibiting specific molecular pathways can restore normal cell function.
To evaluate the potential of combination therapies for leukemia treatment.

Main Methods:

Examined chronic myeloid leukemia (CML) with bcr-abl translocation treated with imatinib mesylate.
Studied acute promyelocytic leukemia (APL) with PML-RAR alpha translocation and retinoic acid treatment.
Investigated acute myeloid leukemia (AML) with FLT3 mutations and farnesyl transferase inhibitors.

Main Results:

Imatinib mesylate inhibits bcr-abl tyrosine kinase, inducing differentiation and apoptosis in CML cells.
Retinoic acids induce degradation of PML-RAR alpha, restoring differentiation in APL.
Inhibition of FLT3 or farnesyl transferase shows potential in AML models.

Conclusions:

Targeted inhibition of specific oncogenic drivers can overcome differentiation block in myeloid leukemias.
Restoring normal differentiation and apoptosis is a viable therapeutic strategy.
Combination therapies targeting multiple genetic lesions may improve leukemia treatment outcomes.