Blast Crisis — Reversing the Direction

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Abstract
The course of chronic myelocytic leukemia (CML) has changed little since the initial description by Minot in 1924.1 In the chronic state there is excessive proliferation of myeloid cells without loss of their capacity to differentiate. Neoplastic transformation occurs at the level of the pluripotent stem cell, with involvement of the myeloid, erythroid, megkaryocytic and lymphoid cell lines. Both cytogenetic and isoenzyme studies have provided evidence that CML is a clonal hematopoietic disorder arising from a single cell. The Philadelphia chromosome, the hallmark of CML, has been demonstrated in all hematopoietic precursor cells.2 , 3 It is an abnormal chromosome 22 in . . .