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[Cancer Research 45, 2456-2461, June 1, 1985]
© 1985 American Association for Cancer Research

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Increased Glucocorticoid Receptor Concentration in Macrophage Differentiation of Myeloid Leukemia Cells with 12-O-Tetradecanoylphorbol-13-acetate1

Hisamaru Hirai2, Tohru Murakami, Akio Urabe and Fumimaro Takaku

The Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo, Tokyo, Japan 113

HL60 cells, human promyelocytic leukemia cells, can be induced to differentiate into more mature myeloid forms by dimethyl sulfoxide (DMSO) or retinoic acid (RA) and into macrophage-like cells by 12-O-tetradecanoylphorbol-13-acetate (TPA) or related compounds. Macrophage differentiation of HL60 cells by TPA treatment induced a 3- to 4-fold increase in glucocorticoid receptor concentration per cell and a 2- to 3-fold increase in glucocorticoid receptor concentration per mg of protein. The ability of TPA derivatives to increase glucocorticoid receptor concentration paralleled their ability to induce macrophage differentiation. Macrophage differentiation of other myeloid leukemia cells by TPA treatment induced a 2- to 3-fold increase in glucocorticoid receptor concentration per cell. Exposure of T-lymphoblasts or erythroleukemia cells to TPA did not affect glucocorticoid receptor concentration. Myeloid differentiation of myeloid leukemia cells by DMSO or RA induced no significant change in glucocorticoid receptor concentration. The increase in glucocorticoid receptor concentration in macrophage differentiation of myeloid leukemia cells with TPA was considered to depend, not on TPA treatment, but on the process of macrophage differentiation. Further, glucocorticoid receptor concentration can be a sensitive marker of macrophage differentiation of myeloid leukemia cells.

1 Supported in part by Grants-in-Aid for Cancer Research from the Ministry of Health and Welfare and from the Ministry of Education, Science, and Culture of Japan.

2 To whom requests for reprints should be addressed, at The Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo, Tokyo, Japan, 113.

Received 1/23/84. Revised 12/31/84. Accepted 2/25/85.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1985 by the American Association for Cancer Research.