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    Tumor antigens: From discovery to vaccine

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    Author
    Huynh, Wally Chau
    Issue Date
    2001
    Keywords
    Health Sciences, Immunology.
    Health Sciences, Oncology.
    Advisor
    Hersh, Evan M.
    
    Metadata
    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    Tumor specific antigens are the holy grails of cancer research. We made an attempt to identify novel tumor antigens by examining the tumor infiltrating B lymphocyte (TIL-B), and lymph node derived B cell (LN-B) population. TIL-B and LN-B cells were tested for reactivity against glutaraldehyde-fixed allogeneic cell lines by enzyme linked immunosorbant assay (ELISA). Of the 466 wells containing TIL-B cells, 29 (6.2%) of them produced antibodies that were reactive to allogeneic tumor cell lines. Of the 712 wells containing LN-B cells, 79 (11.1%) of them produced reactive antibodies to allogeneic tumor cell lines. Unfortunately, we were unable to identify specific clones producing those reactive antibodies by limiting dilution. Furthermore, we examined the murine immune response to a truncated p53 harboring four point mutations and fused to enhanced green fluorescent protein (EGFP). Balb/c mice were immunized with either plasmid DNA or the recombinant protein. We found that delivery by intramuscular injection of plasmid DNA encoding truncated, mutant p53 along with murine GM-CSF mice resulted in non-measurable antibody response and minimal cellular cytotoxic activity while recombinant protein immunization resulted in a strong antibody response and no measurable cytotoxic activity. We conclude that immunization with the fusion construct containing green fluorescent protein does not enhance cytotoxic responses to mutant p53. In addition, the creation of multiple point mutations in the p53 gene may have prevented the fusion protein from being processed and expressed on MHC class I molecules.
    Type
    text
    Dissertation-Reproduction (electronic)
    Degree Name
    Ph.D.
    Degree Level
    doctoral
    Degree Program
    Graduate College
    Cancer Biology
    Degree Grantor
    University of Arizona
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