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Treatment with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) of acute myeloblastic leukemia cells halts proliferation and induces expression of monocyte/macrophage markers. Surface characteristics of leukemic HL60 cells, as defined using a panel of monoclonal antibodies, were found to be similar to those of normal human promyelocytes. TPA treatment, however, induced a phenotype that, unlike normal monocytes, contained several myeloid-specific markers and lacked several monocyte-specific markers. TPA treatment of HL60 cells causes the rapid disappearance of the transferrin receptor from the cell surface. Because transferrin is essential for HL60 cell proliferation in culture, the disappearance of this receptor is followed by an irreversible accumulation of the cells in the G1 phase of the cell cycle. The TPA-induced arrest of cell proliferation suggests the potential of this agent in experimentally treating myeloblastic leukemias.
G Rovera, and
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S Pessano, and
L Bottero, and
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D Lebman
November 1984,
Journal of the National Cancer Institute,
G Rovera, and
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L Bottero, and
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D Lebman
July 1988,
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G Rovera, and
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January 1982,
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July 1983,
Journal of immunology (Baltimore, Md. : 1950),
G Rovera, and
D Ferrero, and
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January 1985,
Medical oncology and tumor pharmacotherapy,
G Rovera, and
D Ferrero, and
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J Vartikar, and
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November 1979,
Cancer research,
G Rovera, and
D Ferrero, and
G L Pagliardi, and
J Vartikar, and
S Pessano, and
L Bottero, and
S Abraham, and
D Lebman
March 1984,
Cancer research,
G Rovera, and
D Ferrero, and
G L Pagliardi, and
J Vartikar, and
S Pessano, and
L Bottero, and
S Abraham, and
D Lebman
January 1982,
Carcinogenesis; a comprehensive survey,
G Rovera, and
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D Lebman
March 1977,
Annals of the New York Academy of Sciences,
G Rovera, and
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D Lebman
October 1984,
International journal of cancer,
