Monoclonal antibodies to carbohydrate antigens in autologous bone marrow transplantation
Article first published online: 19 FEB 2004
Copyright © 1988 Alan R. Liss, Inc.
Journal of Cellular Biochemistry
Volume 36, Issue 4, pages 445–452, April 1988
How to Cite
Ball, E. D. and Howell, A. L. (1988), Monoclonal antibodies to carbohydrate antigens in autologous bone marrow transplantation. J. Cell. Biochem., 36: 445–452. doi: 10.1002/jcb.240360412
- Issue published online: 19 FEB 2004
- Article first published online: 19 FEB 2004
- Manuscript Revised: 5 AUG 1987
- Manuscript Accepted: 5 AUG 1987
- Manuscript Received: 29 MAY 1987
- bone marrow transplantation;
- myeloid cells;
- acute myeloid leukemia
Normal and malignant myeloid cells express a highly immunogenic oligosaccharide, lacto-n-fucopentaose-III (LNF-III), that has been identified by numerous monoclonal antibodies (MoAb). We have been interested in the use of a particular monoclonal antibody to LNF-III, PM-81, in the treatment of patients with acute myelogenous leukemia using the antibody to treat bone marrow in vitro. Following in vitro treatment of bone marrow with PM-81 and another MoAb, AML-2–23, the remaining cells are used as an autograft in a patient treated with high-dose chemotherapy and radiotherapy. In order to enhance the ability of the MoAb to lyse leukemic cells in the remission bone marrow, we have explored the effect of neuraminidase treatment on leukemia cells. In this paper we describe that myeloid leukemia cells expressing low levels of LNF-III by immunofluorescence can be shown to have high levels of LNF-III after neuraminidase treatment. In addition, we show that normal bone marrow progenitor cells do not have cryptic LNF-III antigen, thus allowing the application of this finding to the clinical setting. Moreover, we have shown that leukemia colony-forming cells from one patient with acute myelogenous leukemia express cryptic LNF-III and that after exposure to neuraminidase there was an increased ability of PM-81 in the presence of complement to eliminate these colony forming cells. These data indicate that the LNF-III moiety is almost universally expressed on myeloid leukemia cells and their progenitors but not expressed on normal progenitors. Thus, it may be possible to enhance leukemia cell kill in vitro by neuraminidase treatment of bone marrow.