Abstract

The overall research program proposed here is designed to determine the effectiveness of passive serum therapy to the control of malignant growths. In order to broaden the applicability of the results obtained, several tumor systems are being explored (leukemia, sarcoma, carcinoma) primarily utilizing inbred mice. Special attention is being devoted to two aspects of this problem. First, we are seeking to devise the most efficient and safe protocols by judiciously choosing our target antigens and the corresponding antibodies. Secondly, the underlying mechanisms responsible for successful tumor control or rejection are being actively investigated. Major emphasis is being placed on approaches for immunological management of non-antigenic tumors. We have found that such can be rendered antigenic and responsive to immunological management subsequent to superinfection in situ with viruses. Tumor models are being developed in marmosets in order to extend this approach to primates. Finally, the significance of the elevated levels of IgA in secretions from lung cancer patients is under continuing investigation, as is its value as a diagnostic tool for the disease.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
3P01CA025863-05S1
Application #
3093118
Study Section
Cancer Special Program Advisory Committee (CAK)
Project Start
1980-03-01
Project End
1986-02-28
Budget Start
1984-03-01
Budget End
1986-02-28
Support Year
5
Fiscal Year
1985
Total Cost
Indirect Cost

  Institution

Name
Duke University
Department
Type
Schools of Medicine
DUNS #
071723621
City
Durham
State
NC
Country
United States
Zip Code
27705

  Publications

Hom, R K; Katzenellenbogen, J A (1997) Technetium-99m-labeled receptor-specific small-molecule radiopharmaceuticals: recent developments and encouraging results. Nucl Med Biol 24:485-98
French, A N; Napolitano, E; VanBrocklin, H F et al. (1993) Synthesis, radiolabeling and tissue distribution of 11 beta-fluoroalkyl- and 11 beta-fluoroalkoxy-substituted estrogens: target tissue uptake selectivity and defluorination of a homologous series of fluorine-18-labeled estrogens. Nucl Med Biol 20:31-47
Thiel, K; Genovesi, E V; Iglehart, J D et al. (1988) Loss of tumorigenicity following in vitro MuLV infection is associated with induction of peritoneal natural killer cell activity. Adv Exp Med Biol 239:169-83
Fountzilas, G; Ohnuma, T; Rammos, K et al. (1986) Comparison of mitoxantrone and ametantrone in human acute myelocytic leukemia cells in culture and in bone marrow granulocyte-macrophage progenitor cells. Cancer Drug Deliv 3:93-100
Johnson, W J; Steplewski, Z; Matthews, T J et al. (1986) Cytolytic interactions between murine macrophages, tumor cells, and monoclonal antibodies: characterization of lytic conditions and requirements for effector activation. J Immunol 136:4704-13
Matthews, T J; Weinhold, K J; Langlois, A J et al. (1985) Immunologic control of a retrovirus-associated murine adenocarcinoma. VI. Augmentation of antibody-dependent killing following quantitative and qualitative changes in host peritoneal cells. J Natl Cancer Inst 75:703-8
Palker, T J; Bolognesi, D P; Haynes, B F (1985) Human T-cell leukemia/lymphoma virus: studies of host-virus interaction. Curr Top Microbiol Immunol 115:247-66
Weinhold, K J; Bolognesi, D P; Matthews, T J (1985) Immunologic control of a retrovirus-associated murine adenocarcinoma. VIII. Corynebacterium parvum-activated natural killer cells as potent antibody-dependent cell-mediated cytotoxicity effectors. J Natl Cancer Inst 75:717-24
Langlois, A J; Matthews, T J; Weinhold, K J et al. (1985) Immunologic control of a retrovirus-associated murine adenocarcinoma. VII. Tumor cell destruction by macrophages and IgG2A. J Natl Cancer Inst 75:709-15
Palker, T J; Scearce, R M; Ho, W et al. (1985) Monoclonal antibodies reactive with human T cell lymphotropic virusI (HTLVI) p19 internal core protein: cross-reactivity with normal tissues and differential reactivity with HTLV types I and II. J Immunol 135:247-54

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