Involvement of Arachidonic Acid Metabolites in the Transcriptional Regulation of CSF-1 Gene Expression by Tumor Necrosis Factor

  • M. L. Sherman
  • B. L. Weber
  • R. Datta
  • D. W. Kufe
Part of the Developments in Oncology book series (DION, volume 67)


The macrophage-specific colony stimulating factor (CSF-1) regulates the hematopoietic stem cell formation of monocyte/macrophage-containing colonies (1). CSF-1 also stimulates the production of several biologic factors including prostaglandin E, plasminogen activator, interleukin 1, granulocyte-specific colony stimulating factor, interferon, myeloid colony stimulating activity and tumor necrosis factor (TNF) (2). In contrast to the known pleiotropic effects of CSF-1, the regulation of CSF-1 gene expression has not been extensively examined. Recent studies have demonstrated that phorbol esters and the granulocyte/macrophage-specific colony stimulating factor induce CSF-1 gene expression in MIA-PaCa cells, normal human monocytes, and during monocytic differentiation of human leukemia cells (3–6). Furthermore, the CSF-1 gene has been shown to be constitutively expressed in a variety of human ovarian, breast and lung carcinoma cell lines (7).


Tumor Necrosis Factor Arachidonic Acid Metabolite Lung Carcinoma Cell Line Monocytic Differentiation Tumor Necrosis Factor mRNA 
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Copyright information

© Springer Science+Business Media New York 1991

Authors and Affiliations

  • M. L. Sherman
    • 1
  • B. L. Weber
    • 1
  • R. Datta
    • 1
  • D. W. Kufe
    • 1
  1. 1.Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute and Department of MedicineHarvard Medical SchoolBostonUSA

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