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Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up
Published on: March 26, 2018
Exploring the Origin of Cells in the Progression of Primary Myelofibrosis to Acute Myeloid Leukemia Case Report
Philip Papayanis1, Kara Conroy2, Melissa Larson2
1Department of Medicine, Division of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA, rush.edu.
Abstract:
Primary myelofibrosis (PMF) is the clonal proliferation of common myeloid progenitor (CMP) cells and can transform into acute myeloid leukemia (AML). The exact transformation process and cell lines involved are not well-understood. A patient with PMF received an allogenic hematopoietic stem cell transplant (alloHCT) from his major ABO incompatible sibling and developed pure red cell aplasia that resolved when his blood type switched to that of his donor's. He relapsed with AML 10 months after alloHCT; interestingly, his blood type remained his donor's type. This supports that AML in this patient with PMF stemmed from more committed progenitors (myeloblasts) than CMP.
Insights
Primary myelofibrosis (PMF) can transform into acute myeloid leukemia (AML). A patient
Area of Science:
- Hematology
- Oncology
- Stem Cell Transplantation
Background:
- Primary myelofibrosis (PMF) involves abnormal proliferation of common myeloid progenitor (CMP) cells.
- The transformation of PMF to acute myeloid leukemia (AML) and the specific cell types involved remain unclear.
Purpose of the Study:
- To investigate the cellular origin of acute myeloid leukemia (AML) transformation in a patient with primary myelofibrosis (PMF).
Main Methods:
- Case study of a patient with PMF undergoing major ABO incompatible allogeneic hematopoietic stem cell transplant (alloHCT).
- Monitoring of blood type changes and disease relapse post-transplant.
Main Results:
- The patient experienced pure red cell aplasia, which resolved with blood type conversion to the donor's type.
- Relapse with AML occurred 10 months post-alloHCT, with the blood type remaining the donor's.
Conclusions:
- The AML relapse in this PMF patient likely originated from more committed myeloid progenitors (myeloblasts) rather than CMP.
- This case provides insight into the cellular dynamics of PMF transformation to AML following alloHCT.
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