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Rinsho Byori. 1998 Dec;46(12):1226-31.

[Progress in laboratory medicine in chronic myeloid leukemia].

[Article in Japanese]

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  • 1Third Department of Internal Medicine, Akita University School of Medicine.


Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder that is characterized by splenomegaly and marked elevation of the blood leukocyte count with granulocyte in maturity. Ph chromosome was identified in CML in 1960 and was found to clearly result from reciprocal translocation between chromosome 9 and chromosome 22 (t(q;22)) (q34;q11). CML arises from a single pluripotent hematopoietic stem cell with the Ph chromosome and demonstration of the Ph chromosome in blood or marrow cells establishes and unequivocal diagnosis of CML. The Ph chromosome is recognized as the cytogenetic result of a rearrangement of the ABL gene on chromosome 9 and the BCL gene on chromosome 22, which leads to the creation of a BCR/ABL fusion gene on chromosome 22. Abnormal ABL-related protein with increased tyrosine kinase activity suggested a molecular mechanism of CML. The BCR/ABL fusion gene can be found not only in the chromosome but in interphase nuclei by fluorescence in situ hybridization (FISH). We employed both fluorescence activated cell sorter (FACS) and FISH to study the lineage involvement of individual stem cells and progenitor cells in patients with CML. Evidence of BCR/ABL fusion was found in pluripotent stem cells (CD34+, Thy1+), myeloid cells, B progenitor cells (CD34+, CD19+) and T/NK progenitor cells (CD34+, CD7+, CD5+) but not mature T cells (CD3+) or natural killer cells (CD3-, CD56+). These data suggested that BCR/ABL gene fusion occurs in pluripotent stem cells and that Ph+ T cells and natural killer cells are eliminated during differentiation.

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