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. © 1988 Springer-Verlag.
CITATION STYLE
Simmers, R. N., Smith, J., Shannon, M. F., Wong, G., Lopez, A. F., Baker, E., … Vadas, M. A. (1988). Localization of the human G-CSF gene to the region of a breakpoint in the translocation typical of acute promyelocytic leukemia. Human Genetics, 78(2), 134–136. https://doi.org/10.1007/BF00278182
Mendeley helps you to discover research relevant for your work.