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NATIONAL JEWISH MEDICAL AND RESEARCH CENTER DENVER CO

Overview
Works: 3 works in 6 publications in 1 language and 6 library holdings
Publication Timeline
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Publications about NATIONAL JEWISH MEDICAL AND RESEARCH CENTER DENVER CO
Publications by NATIONAL JEWISH MEDICAL AND RESEARCH CENTER DENVER CO
Most widely held works by NATIONAL JEWISH MEDICAL AND RESEARCH CENTER DENVER CO
Dissecting the Immunogenicity of Monoclonal Antibodies ( file )
3 editions published between 2001 and 2003 in English and held by 3 libraries worldwide
The potential of monoclonal antibodies, (mAbs), for use in therapeutic and diagnostic applications has not been fully realized in part due to counter-immune responses that often arise in patient recipients of mAb. A growing research effort to "humanize" mAb has focused primarily on the structure or sequence of the antibody variable (V) region domains. However, these approaches may ultimately suffer, as they overlook the requirement of T cell help for the immune counter-reaction and the potential of somatic hypermutation and V-D-J recombination to generate target T cell epitopes within mAb V regions. My approach focuses on this issue. In order to understand seine basic principals concerning anti-immunoglobulin immune responses, I have developed a panal of T cell hybridomas, new transgenic mice and a tetrameric staining reagent. Studies with these tools strongly support our basic hypothesis that T cells are tolerant of endogenous immunoglobulin-derived diversity. I have also obtained a panal of T cell hybridomas that are specific for the CDR3 region of a monoclonal antibody supporting our hypothesis that junctional diversity may provide a source of T cell epitopes within a monoclonal antibody. Finally, I have addressed the global nature of T cell responses to junctional diversity with an adoptove transfer system
Cloning and Characterization of Genes That Inhibit TRAIL-Induced Apoptosis of Breast Cancer Cells ( file )
2 editions published between 2003 and 2004 in English and held by 2 libraries worldwide
TRAIL is a tumor necrosis factor family member that can specifically induce apoptosis of cancer cells but not of normal cells. However, some cancer cells are resistant to TRAIL-induced apoptosis. The purpose of this proposed study is to clone and characterize such inhibitory genes of TRAIL-induced apoptosis. Using cDNA subtraction and retroviral cDNA-based expression cloning approaches, we have obtained more than multiple candidate clones of TRAIL-inhibitory genes. Among the candidate clones, the short splice form of Casper/c-FLIP (Casper-S were shown to confer resistance to TRAIL-induced apoptosis. Casper deficient embryonic cells were sensitive to TRAIL-induced apoptosis. Re- introduction of Casper-S into Casper deficient cells conferred resistance to TRAIL-induced apoptosis. This project has identified and validated Casper-S as a major cellular inhibitor of TRAIL-induced apoptosis
Genetic Induction of Cytolytic Susceptibility in Breast Cancer Cells ( Book )
1 edition published in 1999 in English and held by 1 library worldwide
These studies focus on mechanisms by which the E1A oncogene sensitizes tumor cells to destruction by cytolytic lymphocytes and other injuries. The preliminary observation that E1A sensitizes cells to proapoptotic injuries, but not injuries that trigger cellular necrosis has been confirmed. Our speculation that E1A functions independently of the p53 transcription factor has been confirmed. Other studies showed that co-expression of the Bcl-2-like molecule, E1B 19 kD, does not block the E1A sensitizing effect. These data further focus the proposed Tasks. Thus, the search for El A-modulated cellular genes whose altered expression renders cells sensitive to cytolytic injury (Task 1) can now be focused on a p53-independent apoptosis pathway that is not blocked by Bcl-2 activity. RHKO mutagenesis, differential display and PCR-based subtractive hybridization studies have provided limited information on E1A modulation of cellular genes and are being replaced by plans for studies using cDNA chip technology
 
Languages
English (6)
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