Active Immunotherapy in Leukemia With Neuraminidase-Modified Leukemic Cells*
The enzymic cleavage of the terminal sugar residue from the plasma membrane of neoplastic cells by neuraminidase of vibrio cholerae origin causes a marked increase in immunogenicity of most experimental tumors [1–6, 8–16]. In a DBA/2 leukemia L1210 system, a single leukemic cell is capable of producing leukemia and the ultimate death of the host. However, mice which were immunized with neuraminidase-treated leukemia L1210 cells remained protected against a challenge of 100,000 untreated leukemic cells [1–3]. Repeated injections of neuraminidase-treated leukemia L1210 cells reduced the lethality rate and increased survival of mice with leukemia L1210 tumor grafts [15, 16]. Chemotherapy plus neuraminidase-treated L1210 cells administered in a sequence which preserves the host’s immunobiologically competent cells resulted in the cure of a significant portion of immunized mice [4, 7, 9]. The immunoprotection evoked by the stimulation from the neuraminidase-treated tumor cells was specific for the particular tumor and could be transferred by sera or splenic lymphocytes into unimmunized syngeneic mice [5, 7, 15, 16]. Recently, considerable attention has been directed to combined modality therapy in spontaneous Gross virus-induced leukemia in AkR mice because in many respects AkR leukemia has similar characteristics to the human leukemias.
KeywordsPermeability Carbide Lymphoma Leukemia Cyclophosphamide
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