Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention
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[Cancer Research 48, 2524-2430, May 1, 1988]
© 1988 American Association for Cancer Research

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MACG1, a Mouse Monoclonal Antibody Detecting a Monosialoganglioside Expressed in Tumor-infiltrating Macrophages1

Folke Schriever2, Roger D. Dennis, Gert Riethmüller and Judith P. Johnson

Institute of Immunology, University of Munich, D-8000 Munich [F. S., G. R., J. P. J.], and Department of Biochemistry I, University of Marburg, D-3350 Marburg [R. D. D.], West Germany

MacG1 is a mouse monoclonal antibody (mAb) directed against a ganglioside, which is differentially expressed by macrophages infiltrating malignant melanomas and benign melanocytic lesions.

mAb MacG1 was obtained by immunization with liposomes containing a mixture of gangliosides extracted from malignant melanoma. The antibody was selected for binding to melanoma gangliosides and for reactivity with frozen tissue sections of malignant melanoma. mAb MacG1 showed reactivity in 25 of 46 melanomas examined but in only 1 of 51 nevi tested. The mAb did not react with melanoma cells but did with cytoplasmic granules and deposits associated with large dispersed cells, which were also found in some nonmelanomatous tumors and in some lymphoid tissues. Using mAbs directed against differentiation antigens these cells were identified as macrophages. In nearly all reactive tissues MacG1-positive macrophages accounted for a minority of the total macrophages. The difference in reactivity between malignant melanomas and nevi could not be explained by the variable numbers of total macrophages in these lesions. It is suggested that mAb MacG1 may define a functionally distinct subpopulation of tumor-infiltrating macrophages. Staining of cells other than macrophages was observed in some normal and malignant neural tissues. MacG1 bound to a monosialoganglioside extracted from melanoma and reacted only with NeuAc{alpha}2-3Galß1-4Glc-Cer when tested with a panel of ganglioside standards.

1 This work was supported in part by a grant from the Deutsche Krebshilfe, Mildred Scheel Stiftung, Bonn, West Germany.

2 To whom requests for reprints should be addressed, at the Dana-Farber Cancer Institute, Division of Tumor Immunology, 44 Binney Street, Boston, MA 02115, USA.

Received 10/ 9/87. Revised 1/13/88. Accepted 1/26/88.







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 © 1988 by the American Association for Cancer Research.