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Biomedical subjects

C L Reading

Publications and source records attributed to C L Reading.

46 records · Page 3Linked to original sources
PubMed1984

Monoclonal antibodies: the possibilities for cancer therapy.

Previous studies and current efforts to use monoclonal antibodies in human cancer therapy are reviewed. These include antibody-dependent immune reactions in vivo, conjugation of cytotoxic agents to monoclonal antibodies, and monoclonal antibody-mediated tumor cell elimination from bone marrow in vitro for use in autologous bone marrow transplantation. Our studies describe the use of magnetic immunocolloids for the removal of leukemic cells from human bone marrow. Future possibilities for the therapeutic use of monoclonal antibodies are also discussed.

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PubMed1981

In vivo and in vitro production and detection of monoclonal antibodies to surface components on metastatic variants of murine tumor cells.

Mouse-mouse and rat-mouse hybridoma cell lines secreting complement-dependent cytotoxic or cell-binding monoclonal antibodies have been produced against cell surface components of two murine metastatic tumor systems: B16 melanoma and RAW117 lymphosarcoma. We have used both in vivo and in vitro spleen cell culture methods for immunization and have made a number of methodologic alterations to increase the yield and survival of hybridomas including media osmolality, pH, serum type, macrophage feeder layers and supplemented amino acids, vitamins and metabolites. Using complement-dependent cytotoxicity or lectin immobilization of tumor cells to polystyrene via a water-soluble carbodiimide for an enzyme-linked immunosorbant assay we were able to rapidly screen hybridoma cultures for specific antibody secretion.

Animals↗
PubMed1980

Malignancies of metastatic murine lymphosarcoma cell lines and clones correlate with decreased cell surface display of RNA tumor virus envelope glycoprotein gp70.

Variant sublines of the murine lymphosarcoma RAW117 have been derived by sequential cycles of intravenous inoculation of cells and harvesting of solid liver tumors in syngeneic BALB/c mice [Brunson K. W. & Nicolson, G. L. (1978) J. Natl. Cancer Inst. 61, 1499-1503] and also by sequential removal of lectin-reactive cells via repeated adsorption on immobilized-lectins [Reading, C. L. Belloni, P. N. & Nicolson, G. L. (1980) J. Natl. Cancer Inst. 64, 1241-1249]. These cell sublines and their clones were analyzed for abilities to form gross liver tumor metastases after injection intravenously or subcutaneously into syngeneic mice, and this response was related to certain cell surface properties including quantities of viral antigens and lectin-binding sites, exposure of specific cell surface proteins, and quantities of cell surface glycoproteins visualized in gels with 125I-labeled lectins or antibodies. Consistent differences were obtained between RAW117 sublines of low and high malignancy with respect to the amounts or exposures of cell surface glycoprotein components of Mr approximately 70,000 or 69,000 and 71,000, depending on the gel system. Competition radioimmunoassays for RNA tumor virus antigens in the RAW117 lines and clones indicated the presence of Moloney murine leukemic virus antigens gp70, p30, and p12. Enhanced malignancy and metastasis to liver was accompanied by decreases in the cellular contents of viral antigens and loss of gp70 cell surface exposure. Analysis of several clones obtained from sublines selected in vivo and in vitro for high or low malignancy confirmed the inverse relationship between metastasis and expression of gp70 in this system.

Animals↗
PubMedDate not supplied

In vivo and in vitro properties of malignant variants of RAW117 metastatic murine lymphoma/lymphosarcoma.

Using the RAW117 lymphoma/lymphosarcoma system syngeneic to Balb/c strain mice, variant sublines have been selected for enhanced blood-borne liver colonization in vivo or for lack of binding to immobilized lectins in vitro. The kinetic organ distributions of intravenously injected, 3H-thymidine-labelled RAW117 parental cells and a subline sequentially selected ten times for enhanced liver colonization were similar, suggesting that the differences in malignancy between these two cell lines were not due to dramatic differences in organ localization properties. Examination of the malignant properties of the selected sublines and cell clones derived from these in immune-impaired animals indicated that host immune status was important in determining the quantity of experimental metastases in this system. Although impairment of T-cell or NK-mediated anti-tumor responses by using 400 R 60Co-irradiated or Balb/c nude (nu/nu) mice suggested that certain immunologic responses were not effective in preventing experimental metastasis, impairment of macrophage function with chlorine, silica, trypan blue, carrageenan, cyclophosphamide or pristane were effective and resulted in enhanced malignancy of the parental RAW117 line. In contrast, impairment of macrophage function had little or no effect on the experimental metastatic properties of highly malignant RAW117 sublines or clones. In vitro humoral responses or cell-mediated immunologic assays using lymphoid cells from normal or tumor-bearing hosts failed to demonstrate antibody-mediated or antibody-dependent cell-mediated cytotoxicity (ADCC), T-cell or NK-cell responses against RAW117 cells. However, poly I: C activated macrophages were more effective against parental RAW117 cells than against a highly metastatic subline in cytolysis and cytostasis assays suggesting that the highly metastatic RAW117 cells can more readily escape macrophage-mediated host defenses.

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