The concept that acute leukemia is a disease of rapid uncontrolled proliferation of marrow cells was first questioned by Astaldi and Mauri in 1954.1 These investigators cultured marrow from patients with acute leukemia in the presence of colchicine and demonstrated a very low mitotic index. From this simple study the authors concluded that the increased number of primitive cells in the marrow of leukemic patients is the result, not of rapid proliferation, but rather of an accumulation of slowly dividing cells that fail to differentiate. Twelve years later a more sophisticated approach was applied to the study of cellular proliferation in which tritiated thymidine, a radioactive nucleic acid precursor, was administered to patients with acute leukemia.2 These experiments confirmed the observations of Astaldi and Mauri.
All primitive cells within the bone marrow have the same genetic code, but expression of genetic DNA is variable. This variability is accomplished