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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
Chapter
Part of the Developments in Oncology book series (DION, volume 67)

Abstract

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).

Keywords

Tumor Necrosis Factor Arachidonic Acid Metabolite Lung Carcinoma Cell Line Monocytic Differentiation Tumor Necrosis Factor mRNA 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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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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