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[Cancer Research 48, 6424-6428, November 15, 1988]
© 1988 American Association for Cancer Research

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Production of Growth Potentiating Factor(s) for Autologous Blast Cells by Acute Myeloblastic Leukemia Cells1

Ikuo Murohashi2, Kaoru Nagata, Toshiya Suzuki, Yoko Yamashita, Yasuo Maruyama and Nobuo Nara

First Department of Internal Medicine, Tokyo Medical and Dental University, 5-45, Yushima 1-Chome, Bunkyo-ku, Tokyo, 113, Japan

The effects of media conditioned by leukemic cells from 11 acute myeloblastic leukemia patients on the growth of autologous blast progenitors were studied. First, it was shown that T-cell-depleted leukemic cells from some patients release high levels of colony-stimulating activity into the culture medium, whereas following further depletion of phagocytic cells, the levels of colony-stimulating activity become undetectable. Second, media conditioned by purified blast cell fraction depleted of both T-cells and phagocytic cells potentiated autologous blast progenitor growth both in methylcellulose and suspension cultures stimulated by optimal concentration of media conditioned by human bladder carcinoma line 5637. Third, media conditioned by these purified blast cells generally did not contain measurable colony-stimulating activity or interleukin 1, whereas substantial levels of granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, and interleukin 1 were observed in media conditioned by human bladder carcinoma line 5637 using bioassays and specific immunological assays. Therefore, purified blast cell fraction from acute myeloblastic leukemia patients appears to produce factor(s) other than granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, or interleukin 1, which potentiate the growth of autologous blast progenitors both in methylcellulose and suspension cultures.

1 Supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture, Japan.

2 To whom requests for reprints should be addressed.

Received 1/19/88. Revised 5/19/88. Revised 8/15/88. Accepted 8/17/88.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Copyright © 1988 by the American Association for Cancer Research.