ovalbumin and Prostatic-Neoplasms
ovalbumin has been researched along with Prostatic-Neoplasms* in 5 studies
Other Studies
5 other study(ies) available for ovalbumin and Prostatic-Neoplasms
Article | Year |
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Therapeutic ISCOMATRIX™ adjuvant vaccine elicits effective anti-tumor immunity in the TRAMP-C1 mouse model of prostate cancer.
Cancer vaccine development has proven challenging with the exception of some virally induced cancers for which prophylactic vaccines exist. Currently, there is only one FDA approved vaccine for the treatment of prostate cancer and as such prostate cancer continues to present a significant unmet medical need. In this study, we examine the effectiveness of a therapeutic cancer vaccine that combines the ISCOMATRIX™ adjuvant (ISCOMATRIX) with the Toll-like receptor 3 agonist, polyinosinic-polycytidylic acid (Poly I:C), and Flt3L, FMS-like tyrosine kinase 3 ligand. We employed the TRAMP-C1 (transgenic adenocarcinoma of the mouse prostate) model of prostate cancer and the self-protein mPAP (prostatic acid phosphatase) as the tumor antigen. ISCOMATRIX™-mPAP-Poly I:C-Flt3L was delivered in a therapeutic prime-boost regime that was consistently able to achieve complete tumor regression in 60% of animals treated and these tumor-free animals were protected upon rechallenge. Investigations into the underlying immunological mechanisms contributing to the effectiveness of this vaccine identified that both innate and adaptive responses are elicited and required. NK cells, CD4 Topics: Adjuvants, Immunologic; Animals; Antigens, Neoplasm; Apoptosis; Cancer Vaccines; CD8-Positive T-Lymphocytes; Cell Proliferation; Cholesterol; Disease Models, Animal; Drug Combinations; Humans; Interferon-gamma; Male; Melanoma, Experimental; Membrane Proteins; Mice; Mice, Inbred C57BL; Ovalbumin; Phospholipids; Poly I-C; Prostatic Neoplasms; Saponins; Tumor Cells, Cultured; Tumor Microenvironment; Xenograft Model Antitumor Assays | 2020 |
Reprogramming Immune Response With Capsid-Optimized AAV6 Vectors for Immunotherapy of Cancer.
In the current studies we generated novel capsid-optimized adeno-associated virus (AAV) serotype 6 (AAV6) vectors expressing a tumor-associated antigen, and assessed their ability to activate a protective T-cell response in an animal model. First, we showed that specific mutations in the AAV6 capsid increase the transduction efficiency of these vectors in mouse bone marrow-derived dendritic cells in vitro for approximately 5-fold compared with the wild-type (WT) AAV6 vectors. Next, we evaluated the ability of the mutant AAV6 vectors to initiate specific T-cell clone proliferation in vivo. Our data indicate that the intramuscular administration of AAV6-S663V+T492V vectors expressing ovalbumin (OVA) led to a strong activation (approximately 9%) of specific T cells in peripheral blood compared with AAV6-WT treated animals (<1%). These OVA-specific T cells have a superior killing ability against mouse prostate cancer cell line RM1 stably expressing the OVA antigen when propagated in vitro. Finally, we evaluated the ability of capsid-optimized AAV6-S663V+T492V vectors to initiate a protective anticancer immune response in vivo. Our results document the suppression of subcutaneous tumor growth in animals immunized with AAV6-S663V+T492V vectors expressing prostatic acid phosphatase (PAP) for approximately 4 weeks in comparison with 1 week and 2 weeks for the negative controls, AAV6-EGFP, and AAV6-WT-PAP treated mice, respectively. These studies suggest that successful inhibition of tumor growth in an animal model would set the stage for potential clinical application of the capsid-optimized AAV6-S663V+T492V vectors. Topics: Animals; Capsid; Capsid Proteins; Cell Line, Tumor; Dependovirus; Genetic Therapy; Genetic Vectors; Immunotherapy; Male; Mice; Mice, Inbred C57BL; Neoplasms; Ovalbumin; Prostatic Neoplasms; T-Lymphocytes; Transduction, Genetic | 2015 |
Dual antigen target-based immunotherapy for prostate cancer eliminates the growth of established tumors in mice.
We have previously shown that immunization with an adenovirus vector carrying an individual antigen induces antigen-specific CD8 T cells actively engaged in the destruction of tumor cells expressing the cognate antigen. In order to expand the range of antitumor responses beyond an individual antigen, we designed a recombinant adenovirus type 5 (rAd5) carrying a fusion construct of two full-length antigens. We used this adenovirus vector to test the concept that multiantigenic effector T cells could be generated simultaneously following a single immunization.. To perform the rAd5 constructs, we selected a combination of prostate-specific antigen (PSA) and prostate stem cell antigen (PSCA) genes based on their restricted distribution within the prostate tissue and their association with the development and progression of prostate cancer.. Immunization of mice with rAd5 vector carrying a fusion construct of PSA and PSCA (Ad5-PSA/PSCA) simultaneously induced the expansion of anti-PSA and anti-PSCA CD8 T cells, as measured by intracellular cytokine staining for IFN-γ. The antigen-specific T-cell responses that developed were efficient in eliminating the target cells expressing cognate antigens measured by an in vivo cytotoxic T-cell assay. The in vivo tumor growth study showed that immunization of mice with Ad5-PSA/PSCA vaccine induced strong antitumor immunity when challenged with mouse prostate tumor cell lines (RM11) expressing human PSA (RM11/PSA). To further analyze the impact on therapeutic efficacy of Ad5-PSA/PSCA vaccine against the tumor cells expressing PSA and PSCA (RM11-PSA/PSCA) antigens, we injected mice with Ad5-PSA/PSCA vaccine. The vaccine inhibited the growth of established tumors with 80% of the mice becoming tumor free. These data provide useful information that antigen-specific effector T cells can be generated simultaneously and that their additive antitumor effect has the potential to eliminate the growth of established tumors. Therefore, the immunotherapy approach of using the simultaneous targeting of dual antigens associated with prostate cancer may have important implications for human clinical trials. Topics: Adenoviridae; Animals; Antigens, Neoplasm; Cancer Vaccines; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Cytotoxicity Tests, Immunologic; Dendritic Cells; Epitopes, T-Lymphocyte; GPI-Linked Proteins; Humans; Immunotherapy, Active; Interferon-gamma; Lymphocyte Activation; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Neoplasm Proteins; Ovalbumin; Prostate-Specific Antigen; Prostatic Neoplasms; Spleen; T-Lymphocytes, Cytotoxic; Transfection; Vaccines, DNA; Xenograft Model Antitumor Assays | 2011 |
Immunization against luteinizing hormone-releasing hormone fusion proteins does not decrease prostate cancer in the transgenic adenocarcinoma mouse prostate model.
This study was undertaken to test the effect of immunization against luteinizing hormone-releasing hormone (LHRH) fusion proteins on the development and progression of prostate cancer in the transgenic adenocarcinoma mouse prostate (TRAMP) model. Two LHRH fusion proteins, ovalbumin with seven LHRH peptides (OV-LHRH-7), and thioredoxin with seven LHRH peptides (TH-LHRH-7) were used in a cocktail vaccine. Two groups of male TRAMP mice were immunized with the cocktail. Primary immunizations were at either 4 or 8 weeks of age. LHRH immunized mice (n=19) were compared with castrated (n=19) and intact mice (n=18) for testosterone concentration, tumor weight, and lifespan. Immunization against LHRH in the TRAMP mice resulted in significant production of antibodies to LHRH compared with surgically castrated and intact control mice. Testicular weight was significantly reduced in the LHRH immunized groups compared with intact control mice. Serum testosterone was reduced (P<0.05) in the immunized mice compared with intact control mice and was not different from that of castrated mice (P>0.05). Tumor weight was variable and inconsistent throughout all treatment groups. Lifespan was not increased by immunization against LHRH or castration. Intact control mice (lived the longest (227+/-11 days), whereas immunized mice lived 206+/-11 days and castrated mice lived 213+/-13 days. Tumors from immunized TRAMP mice appeared more aggressive than tumors of castrated and intact mice, as demonstrated by 35% expression of gross lung tumors in the immunized mice whereas none were observed in the castrated or intact TRAMP mice. Prostate cancer is initially dependent upon androgens for growth and development, but cells have the ability to escape androgen dependence and progress to an androgen independent state, which was evident in this study. The TRAMP mouse model immunized against LHRH may have utility in future studies and treatments of the androgen independent prostate cancer. Topics: Adenocarcinoma; Animals; Disease Models, Animal; Disease Progression; Gonadotropin-Releasing Hormone; Immunization; Male; Mice; Mice, Inbred C57BL; Neoplasm Metastasis; Orchiectomy; Organ Size; Ovalbumin; Prostatic Neoplasms; Recombinant Fusion Proteins; Testis; Testosterone; Thioredoxins | 2003 |
Characterization of cytolytic effector cells in peripheral blood of healthy individuals and cancer patients. II. Cytotoxicity to allogeneic or autochthonous tumor cells in tissue culture.
Topics: Carcinoma, Transitional Cell; Cell Separation; Cells, Cultured; Cytotoxicity Tests, Immunologic; Female; Humans; Immunity, Cellular; Immunosorbent Techniques; Lymphocytes; Male; Ovalbumin; Prostatic Neoplasms; Urinary Bladder Neoplasms | 1977 |