Localization of the human G-CSF gene to the region of a breakpoint in the translocation typical of acute promyelocytic leukemia |
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Authors: | R. N. Simmers J. Smith M. F. Shannon G. Wong A. F. Lopez E. Baker G. R. Sutherland M. A. Vadas |
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Affiliation: | (1) Cytogenetics Unit, Adelaide Children's Hospital, King Wiliam Road, 5006 North Adelaide, S.A., Australia;(2) Division of Human Immunology, Institute of Medical and Veterinary Science, Frome Road, 5000 Adelaide, S.A., Australia;(3) Genetics Institute, 02115 Boston, MA, USA |
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Abstract: | Summary The colony-stimulating factors regulate growth, differentiation, and function of blood cells. The effect of granulocyte colony-stimulating factor (G-CSF) on myeloid leukemias is unique among colony-stimulating factors in driving the leukemic cells from a self-renewing malignant state to a mature differentiated phenotype with the concomitant loss of tumorigenicity. This property of G-CSF has led to suggestions that its absence is responsible for lack of differentiation of leukemic cells and that the therapeutic administration of G-CSF could reverse this defect and result in a cure for leukemia. Here we show that the gene coding for human G-CSF is localized to chromosome 17, bands q11.2-21. The translocation of the long arm of chromosome 17 at q12-21 to chromosome 15 is a specific abnormality occurring in a high proportion of, if not all, patients with acute promyelocytic leukemia, a disease characterized by undifferentiated myeloid cells and a dismal prognosis. Abnormalities of the regulation of a specific differentiation factor gene mediated by a specific chromosomal rearrangement may be directly implicated in the pathogenesis of human leukemia. |
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