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[Cancer Research 43, 491-495, February 1, 1983]
© 1983 American Association for Cancer Research

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Cell Growth-dependent Variation in the Sensitivity of Human and Mouse Tumor Cells to Complement-mediated Killing1

S. H. Ohanian2, M. Yamazaki3, S. I. Schlager4 and M. Faibisch5

Laboratory of Immunobiology, National Cancer Institute, NIH, Bethesda, Maryland 20205

2 To whom requests for reprints should be addressed, at Laboratory of Immunobiology, National Cancer Institute, NIH, 9000 Rockville Pike, Building 37, Room 2B15, Bethesda, Md. 20205.

Cells removed from asynchronous cultures during lag, log, and stationary phases of growth were found to differ in their sensitivity to antibody/complement-mediated killing. The human lymphoblastoid line, Raji, was relatively more susceptible to killing by human anti-HLA antibody plus rabbit complement during the lag and log phases of growth, while the human lymphoid cell line, PY, was relatively more susceptible to rabbit antilymphocyte serum or human anti-HLA plus rabbit complement during the log and late-log phases of growth. The mouse mastocytoma cell line, P815, was relatively resistant to killing by rabbit anti-P815 plus guinea pig complement during the middle log phase of growth. The variation in sensitivity of the three cell lines was dependent upon the concentration of antibody used to sensitize the cells but not due to differences in antigen expression, antigen density, or net synthesis of DNA, RNA, protein, complex carbohydrate, or lipid-containing macromolecules.

These data suggest that the variability in susceptibility of the cells for complement-mediated killing is due to changes in physiological and/or physicochemical properties of the cells which either affect the ability of the cells to repair complement-mediated damage or nullify the activity of cell-bound complement.

1 Presented in part at Sapparo Cancer Seminar Symposium, "Escape of Tumor Cells from Immune Controls," July 15, 1981, Sapporo, Japan. This is Paper 25 in the series, "Lysis of Tumor Cells by Antibody and Complement."

3 Present address: Faculty of Pharmaceutical Sciences, Teikyo University, Sagamiko, Kanagawa, 199-01, Japan.

4 Present address: Department of Microbiology, University of Notre Dame, Notre Dame, Ind. 46556.

5 Present address: Yale University, New Haven, Conn.

Received 4/ 5/82. Accepted 11/ 1/82.







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 © 1983 by the American Association for Cancer Research.