Disturbed regulation of genes controlling leukomo-genesis frequently underlays hematologic malignancies. Some 50 years ago, Nowell and Hungerford [1961] discovered in leukemic cells of patients with chronic myeloge-nous leukemia that a G-group chromosome had been replaced by a small and characteristic acrocentric chromosome, named after the location of the authors, the Philadelphia chromosome (Ph1). This discovery suggested that an acquired chromosomal rearrangement may lead to a disease involving clonal expansion of a genetically altered cell, which no longer adequately responded to normal controls of cell proliferation and differentiation.
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