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[Cancer Research 51, 612-618, January 15, 1991]
© 1991 American Association for Cancer Research

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In Vivo Acquisition of Fc{gamma}RII Expression on Polyoma Virus-transformed Cells Derived from Tumors of Long Latency1

M. Ran, B. Katz, N. Kimchi, E. Halachmi, J-L. Teillaud, J. Even, Y. Berko-Flint, E. Atlas, W. H. Fridman and I. P. Witz

Department of Microbiology and the Moise and Frida Eskenasy Institute for Cancer Research, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel [M. R., B. K., N. K., E. H., Y. B-F, E. A., I. P. W.], and Laboratoire d'Immunologie Celluaire et Clinique, INSERM U. 255, Institute Curie, Paris, France [J-L. T., J. E., W. H. F.]

BALB/c3T3 cells transformed in vitro with polyoma virus were cloned and passaged once in syngeneic mice. Resulting tumors from each clone were explanted and recultured. Expression of receptor for Fc of IgG (Fc{gamma}RII) in the original in vitro maintained clones and in cells derived from tumors elicited by the respective cells was measured at the protein level as well as at the mRNA level. Clones were assayed in pairs. The ancestor in vitro maintained clones [designated cultured cells (C)] were compared with cells derived from the same clones after a single passage in vivo followed by explanation and reculturing [designated cultured-tumor-cultured cells (CTC)]. C cells of any of the tested clones did not express Fc{gamma}RII. On the other hand, certain CTC cells were positive. The Fc{gamma}RII-positive cells were derived from tumors appearing after a long precancer latency period (>140 days). CTC cells derived from tumors that appeared after shorter latency periods (<80 days) were Fc{gamma}RII negative. These results were obtained both by using radioimmunoassay and monoclonal antibodies against mouse Fc{gamma}RII as well as by Northern blot analysis using the Fc{gamma}RII complementary DNA probe. The involvement of macrophages as the Fc{gamma}RII-expressing cells in CTC cells was excluded.

Fc{gamma}RII expression was down-regulated in CTC cells as a function of time following their explantation into culture. Fc{gamma}RII expression could be up-regulated in these cells and induced on C cells by maintaining the cultured cells in the presence of normal mouse serum or recombinant interferon. We also tested the expression of Fc{gamma}RII on CTC cells following their inoculation into syngeneic mice for a second time (CTCx2 cells). The results showed a positive correlation between Fc{gamma}RII expression in the inoculated ancestor CTC cells and on the CTCx2 cell progeny.

1 This work has been supported by the Israel Cancer Association, Tel Aviv; the National Council for Research and Development, Jerusalem; Association pour la Recherche sur le Cancer, Paris; Concern Foundation, Los Angeles; The Fainbarg Family Fund, Orange County; and the Mary A. Pikovski Fund, Jerusalem. Yehudit Berko-Flint is a fellow of the Israel Cancer Research Fund and Isaac P. Witz is the incumbent of the David Furman Chair in Immunobiology of Cancer.

Received 5/30/90. Accepted 10/26/90.







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
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1991 by the American Association for Cancer Research.