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[Cancer Research 41, 4781-4785, November 1, 1981]
© 1981 American Association for Cancer Research

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Classification of Human Leukemia by Membrane Antigen Analysis with Xenoantisera1

Richard S. Metzgar2, Barry L. Dowell3, Lawrence B. Lachman, Nancy H. Jones and Frederick W. George, IV

Department of Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina 27710 [R. S. M., B. L. D., L. B. L., N. H. J., F. W. G.], and Yerkes Primate Research Center, Emory University, Atlanta, Georgia 30322 [R. S. M.]

Rabbit and monkey antisera after appropriate absorption were rendered specific for normal or leukemic lymphoid- and myeloid-associated antigens. Antisera defining a common peripheral blood T-cell antigen, a thymus leukemia antigen, HLA-DR or la-like antigen, common acute lymphoblastic leukemia antigen (CALLA), and a myeloid-monocyte (M) antigen were used in a microcytotoxicity assay to classify leukemic cells from 30 patients in a double blind study. The antisera to the M antigen reacted with adherent peripheral blood cells and polymorphonuclear leukocytes and failed to react with nonadherent mononuclear cells and enriched T-cells and chronic lymphocytic leukemia cells. The M antisera also reacted with U937, a monocytic-type cell line, and with HL60, a promyelocytic-type cell line, but failed to react with T and B lymphoblastoid cell lines. The specificities of the other antisera have been described in previous reports.

Cells from three of the patients could not be phenotyped by microcytotoxicity testing. Cells from 25 patients had a consensus morphological or histochemical diagnosis of either acute lymphoblastic leukemia or acute nonlymphocytic leukemia. The serological classification of these patients using the five types of antisera listed above were consistent with the consensus diagnosis. In addition, the lymphoid cancers were further subclassified as to T-, B-, or thymus antigen types. There was no consensus lymphoid versus myeloid diagnosis on cells from two patients. The serological classification in both cases favored a diagnosis of myeloid rather than lymphoid leukemia.

1 Presented at the Conference on Cell Markers in Acute Leukemia, March 4 and 5, 1980, Bethesda, Md. Supported by USPHS Grants CA 15525, CA 08975, and CA 11265 from the National Cancer Institute and Grant AM 08054 from the National Institute of Arthritis, Metabolism, and Digestive Diseases to Duke University. Production of primate antisera was partially supported by Grant FR 00165 from the Division of Research Resources to Yerkes Primate Research Center.

2 To whom requests for reprints should be addressed, at Department of Microbiology and Immunology, Duke University Medical Center, Durham, N. C. 27710.

3 Special Fellow of the Leukemia Society of America.







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 © 1981 by the American Association for Cancer Research.