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Cancer Institute, 481 Little Lonsdale St., Melbourne, 3000, [S. H., J. R.], and Australia Department of Pathology, University of Melbourne, Parkville 3052, [I. F. C. M.] Australia
A xenoantiserum raised against a mast cell tumor line (FMP1.1) was found to have cross-reactivity with surface antigens on primitive hemopoietic precursor cells in normal mouse bone marrow: erythroid burst-forming units; granulocyte-macrophage colony-forming cells; and high-proliferative-potential granulocyte-macrophage colony-forming cells. In the presence of anti-FMP1.1 serum and complement, only 15 ± 2% (S.E.) (n = 5) of normal nucleated marrow cells were lysed, demonstrating that the majority of mature hemopoietic cells did not express the antigens detected on their primitive counterparts. A variety of hemopoietic and other tumor cell lines were examined with anti-FMP1.1 serum, and all B- and pre-B-lymphomas, one plasmacytoma, one mastocytoma, and a monocyte-macrophage line exhibited significant lysis. Direct typing of the FMP1.1 tumor demonstrated that it did not express the B-cell surface antigens such as la, surface immunoglobulin, Fc, and complement (C3) receptors. Although the Ly.6 alloantigen was present on FMP1.1 cells, this antigen was not found on marrow erythroid burst-forming units and granulocyte-macrophage colony-forming units. Absorption of anti-FMP1.1 serum with cross-reacting (WEHI-3 and W-279.1) and a nonreacting (P-815) cell line confirmed the specificity of the antiserum reaction with these cells and marrow progenitors. These experiments indicated that more than one antibody is contained in anti-FMP1.1 serum. Thus, the mast cell tumor (FMP1.1) carries an unusual array of antigens, which are found on bone marrow progenitors and are not expressed on the majority of differentiated cells. It has been demonstrated that tumor cell lines provide an important basis for the analysis of surface membrane antigens expressed on normal hemopoietic progenitors.
1 Supported by the National Health and Medical Research Council (Australia) and Grant CA-22080 from the National Cancer Institute, NIH, Bethesda, Md.
Received 1/ 9/81. Accepted 6/ 3/81.
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