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Expression of the Macrophage Growth Factor, CSF-1 and Its Receptor c-fms by a Hodgkin's Disease-derived Cell Line and Its Variants¹

Department of Oncology, Montefiore Medical Center [E. P., J. R., P. H. W.], and Departments of Medicine, Division of Oncology, of Developmental Biology and Cancer [E. R. S.], and of Pathology [P. P.], Albert Einstein College of Medicine, Bronx, New York 10467, and Department of Medicine, Hematology/Lymphoma Service, Memorial Sloan Kettering Cancer Center, New York, New York 10021 [M. A.]

Expression of the macrophage colony-stimulating factor CSF-1 and its receptor, the product of the protooncogene c-fms, was detected in cell line L428, originally derived from a patient with nodular sclerosis Hodgkin's disease, and its two sublines L428KS and L428KSA. While all lines expressed membrane-associated and soluble CSF-1 proteins, L428KSA secreted 30-fold greater amounts of CSF-1 than the other cells. Three transcripts for CSF-1 (4.4, 3.7, 3.4 kilobases) were expressed in all lines and an additional 2.1-kilobase message in L428KSA. Restriction enzyme fragment analysis did not reveal any gross rearrangements of the CSF-1 gene. L428 and L428KS contained a 4.4-kilobase message for c-fms, whereas L428KSA expressed a smaller 3.8-kilobase c-fms transcript. The c-fms gene structure appeared to be unaltered in all lines by restriction enzyme fragment pattern analysis. Monoclonal anti-c-fms antibody precipitated from all cells a M_r 120,000/130,000 doublet and two lower molecular weight phosphoproteins; however, only L428KSA cells showed evidence for an autocrine growth regulation by CSF-1. DNA ploidy and proliferation kinetic studies suggested that L428KSA were derived from the actively proliferating mononuclear Hodgkin's cell population of the parental cell line. Since the simultaneous expression of CSF-1 and c-fms is a characteristic feature of mononuclear phagocytes, these results suggest that Hodgkin's cells are affiliated with the monocyte/macrophage lineage or, at least, derived from a hemopoietic cell type with the capability for aberrant expression of a monocyte-specific growth factor and its receptor.

¹ This work was supported by the Albert Einstein College of Medicine Cancer Core Grant (P30CA13330) awarded by the National Cancer Institute, Department of Health and Human Services, a Henry and Lillian Stratton Foundation grant and by the Chemotherapy Foundation (to E. P.), by NIH Grant CA43864 (to J. R.), by NIH Grants CA26504 and CA32551 (to E. R. S.), and by NIH Grants CA41305 and CA38980 (to M. A.).

² To whom requests for reprints should be addressed, at Department of Oncology, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467.

Received 8/31/89. Revised 11/29/89.

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