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  • CELL  (34)
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  • 1
    Keywords: VACCINE ; vaccination ; TRENDS ; DANGER ; danger signal ; BIOLOGY ; SIGNAL ; virus ; CELL ; tumor ; SURVIVAL ; CANCER ; VOLUME ; INFECTION ; PHASE-II
    Type of Publication: Book chapter
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  • 2
    Keywords: MEMORY ; virus ; ACTIVATION ; PATIENT ; CELLS ; CANCER ; SURVIVAL ; tumor ; TUMOR-CELLS ; THERAPY ; human ; PATIENT SURVIVAL ; HUMAN CANCER ; HUMAN CANCERS
    Type of Publication: Book chapter
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  • 3
    Keywords: brain ; CELLS ; EXPRESSION ; SURVIVAL ; tumor ; TUMOR-CELLS ; BLOOD ; CELL ; Germany ; THERAPY ; DISEASE ; LONG-TERM ; TUMORS ; TIME ; PATIENT ; INFECTION ; prognosis ; SKIN ; T cell ; T cells ; T-CELL ; T-CELLS ; cell culture ; culture ; MEMORY ; virus ; NERVOUS-SYSTEM ; NO ; immunohistochemistry ; ASSAY ; NUMBER ; VACCINE ; SAFETY ; CD8(+) ; immune response ; IMMUNE-RESPONSE ; IMMUNITY ; T-LYMPHOCYTES ; vaccination ; T lymphocyte ; side effects ; NEWCASTLE-DISEASE VIRUS ; ESTABLISHMENT ; TUMOR CELLS ; LONG-TERM SURVIVORS ; GLIOMAS ; T lymphocytes ; IMMUNIZATION ; ONCOLOGY ; AUTOLOGOUS TUMOR ; overall survival ; NEWCASTLE-DISEASE-VIRUS ; SURVIVORS
    Abstract: Purpose Prognosis of patients with glioblastoma is poor. Therefore, in glioblastoma patients, we analyzed whether antitumor vaccination with a virus-modified autologous tumor cell vaccine is feasible and safe. Also, we determined the influence on progression-free survival and overall survival and on vaccination-induced antitumor reactivity. Patients and Methods In a nonrandomized study, 23 patients were vaccinated and compared with nonvaccinated controls (n = 87). Vaccine was prepared from patient's tumor cell cultures by infection of the cells with Newcastle Disease Virus, followed by gamma-irradiation, and applied up to eight times. Antitumor immune reactivity was determined in skin, blood, and relapsed tumor by delayed-type hypersensitivity skin reaction, ELISPOT assay, and immunohistochemistry, respectively. Results Establishment of tumor cell cultures was successful in approximately 90% of patients. After vaccination, we observed no severe side effects. The median progression-free survival of vaccinated patients was 40 weeks (v 26 weeks in controls; log-rank test, P =.024), and the median overall survival of vaccinated patients was 100 weeks (v 49 weeks in controls; log-rank test, P 〈.001). Forty-five percent of the controls survived 1 year, 11% survived 2 years, and there were no long-term survivors (greater than or equal to3 years). Ninety-one percent of vaccinated 39% survived 2 years, and 4% were long-term survivors. In the patients survived I year, vaccinated group, immune monitoring revealed significant increases of delayed-type hypersensitivity reactivity, numbers of tumor-reactive memory T cells, and numbers of CD8(+) tumor-infiltrating T-lymphocytes in secondary tumors. Conclusion Postoperative vaccination with virus-modified autologous tumor cells seems to be feasible and safe and to improve the prognosis of patients with gliobiastomas. This could be substantiated by the observed antitumor immune response. (C) 2004 by American Society of Clinical Oncology
    Type of Publication: Journal article published
    PubMed ID: 15452186
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  • 4
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; CELL ; SYSTEM ; TOOL ; GENE ; cell line ; TRANSDUCTION ; INFECTION ; murine ; recombination ; antibodies ; antibody ; TARGET ; virus ; MOUSE ; hormone ; VECTORS ; CELL-LINE ; FUSION ; LINE ; CARCINOMA-CELLS ; MAMMALIAN-CELLS ; HEMATOPOIETIC PROGENITOR CELLS ; RETROVIRAL VECTORS ; VIRAL VECTORS ; PLASMID DNA ; TRANSGENE EXPRESSION ; HIGH-TITER ; gene transfer,ES cells,MESV retroviral vectors,adenoviral vectors,Cre recombinase,Cre.PR fusion ; RECOMBINANT ADENOVIRUS ; SOMATIC MUTAGENESIS
    Abstract: Background Genetic modification of embryonic stem (ES) cells represents a powerful tool for transgenic and developmental experiments. We report that retroviral constructs based on murine embryonal stem cell virus (MESV) can efficiently deliver and express Cre recombinase or a post-translationally inducible Cre-Progesterone receptor (Cre.PR) fusion in mouse fibroblasts and ES cells.Methods To study the vectors a sensitive reporter cell line, 3TZ, was derived from the murine 3T6 fibroblast line that expresses beta-galactosidase only upon Cre-mediated recombination. This was used together with the ROSA26-R ES cell Cre-reporter system or unmodified mouse ES cells as targets of infection. Efficiency of gene transfer was evaluated immunohistochemically by the use of an anti-Cre polyclonal antibody, and by monitoring the expression of beta-galactosidase.Results Infection of the 3TZ cells with high titer 718C or 719CP virus revealed efficient gene transduction of constitutive or hormone-inducible recombinase activity, respectively. The vectors efficiently transduced murine ES cells with Cre, Cre-PR (fusion of Cre and progesterone receptor) or beta-galactosidase. Cre-mediated recombination in more than 60% of ROSA26-R ES cells was achieved when infected by a VSV-G-pseudotyped MESV retrovirus at MOI of 50.Conclusions The MESV-based retroviral systems, when combined with hormone inducible Cre, represent efficient tools for the transfer of Cre activity in ES cells. Copyright (C) 2004 John Wiley Sons, Ltd
    Type of Publication: Journal article published
    PubMed ID: 14716675
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  • 5
    Keywords: CANCER ; CELLS ; EXPRESSION ; Germany ; IN-VIVO ; ADHESION MOLECULES ; MICE ; COMPLEX ; COMPLEXES ; tumour ; ANTIGEN ; CONTRAST ; DENDRITIC CELLS ; T-CELL ; T-CELLS ; FREQUENCY ; MOLECULE ; bone marrow ; BONE-MARROW ; virus ; LINE ; ADHESION ; NAIVE ; ADHESION MOLECULE ; EFFECTOR ; adoptive immunotherapy ; FEATURES ; RE ; CLASS-II ; PROTECTIVE IMMUNITY ; memory T cells ; PERSISTENCE ; CD8(+) T-cell memory ; GAMMA-IRRADIATION ; LYMPHOCYTES-T ; tumour dormancy
    Abstract: LacZ (Gal)-reactive immune cells were transferred into athymic nu/nu mice inoculated with Gal-expressing syngeneic tumour cells (ESbL-Gal) in order to study tumour-protective T-cell memory. This transfer prevented tumour outgrowth in recipients and resulted in the persistence of a high frequency of Gal-specific CD8(+) T cells in the bone marrow and spleen. In contrast, such Ag-specific memory CD8(+) T cells were not detectable by peptide-major histocompatibility complex (MHC) multimer staining in animals that had not previously received an antigenic challenge. Even though CD44(hi) memory T cells from the bone marrow showed a significantly higher turnover rate, as judged by bromodeoxyuridine (BrdU) incorporation, than respective cells from spleen or lymph nodes, as well as in comparison to CD44(lo) naive T cells, these findings suggest that tumour-associated antigen (TAA) from residual dormant tumour cells are implicated in maintaining high frequencies of long-term surviving Gal-specific memory CD8(+) T cells. Memory T cells could be recruited to the peritoneal cavity by tumour vaccination of immunoprotected nu/nu mice and exhibited ex vivo antitumour reactivity. Long-term immune memory and tumour protection could be maintained over four successive transfers between tumour-inoculated recipients, which involved periodic antigenic restimulation in vivo prior to reisolating the cells for adoptive transfer. Using a cell line (ESbL-Gal-BM) that was established from dormant tumour cells isolated from the bone marrow of immunoprotected animals, it could be demonstrated that the tumour cells had up-regulated the expression of MHC class I molecules and down-regulated the expression of several adhesion molecules during the in vivo passage. Our results suggest that the bone marrow microenvironment has special features that are of importance for the maintenance of tumour dormancy and immunological T-cell memory, and that a low level of persisting antigen favours the maintenance of Ag-specific memory T cells over irrelevant memory T cells
    Type of Publication: Journal article published
    PubMed ID: 15946250
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  • 6
    Keywords: CANCER ; CELLS ; SURVIVAL ; tumor ; TUMOR-CELLS ; Germany ; MODEL ; MODELS ; THERAPY ; PATIENT ; ACTIVATION ; RESPONSES ; INFECTION ; ANTIGEN ; DENDRITIC CELLS ; T-CELL ; T-CELLS ; bone marrow ; BONE-MARROW ; IMMUNE-RESPONSES ; virus ; TRIAL ; CLINICAL-TRIALS ; LONG-TERM SURVIVAL ; Jun ; VACCINE ; IMMUNE-RESPONSE ; IMMUNOTHERAPY ; INTERFERON-ALPHA ; CANCER PATIENTS ; tumor vaccine ; APOPTOSIS-INDUCING LIGAND ; PHASE-II ; STANDARD ; RE ; PATIENT SURVIVAL ; ACTIVE-SPECIFIC IMMUNOTHERAPY ; NEWCASTLE-DISEASE-VIRUS ; DELAYED-TYPE HYPERSENSITIVITY ; dendritic cell ; PHASE ; Newcastle disease virus ; tumor-antigen ; memory T cells ; phase II ; COLORECTAL-CANCER PATIENTS ; METASTATIC SPREAD ; POSTOPERATIVE IMMUNOTHERAPY
    Abstract: For active specific immunotherapy of cancer patients, we designed the autologous virus-modified tumor cell vaccine ATV-NDV. The rationale of this vaccine is to link multiple tumor-associated antigens (TAAs) from individual patient-derived tumor cells with multiple danger signals (DS) derived from virus infection (dsRNA, HN, IFN-alpha). This allows activation of multiple innate immune responses (monocytes, dendritic cells, and NK cells) as well as adaptive immune responses (CD4 and CD8 memory T cells). Preexisting antitumor memory T cells from cancer patients could be activated by antitumor vaccination with ATV-NDV as seen by augmentation of antitumor memory delayed-type hypersensitivity (DTH) responses. In a variety of phase II vaccination studies, an optimal formulation of this vaccine could improve long-term survival beyond what is seen in conventional standard therapies. A new concept is presented which proposes that a certain threshold of antitumor immune memory plays an important role (1) in the control of residual tumor cells which remain after most therapies and (2) for long-term survival of treated cancer patients. This immune memory is T-cell based and most likely maintained by persisting TAAs from residual dormant tumor cells. Such immune memory was prominent in the bone marrow in animal tumor models as well as in cancer patients. Immunization with a tumor vaccine in which individual TAAs are combined with DS from virus infection appears to have a positive effect on antitumor immune memory and on patient survival
    Type of Publication: Journal article published
    PubMed ID: 15838708
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  • 7
    Keywords: CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; BLOOD ; Germany ; human ; DISEASE ; ENZYMES ; GENOME ; RNA ; LINES ; RESPONSES ; INFECTION ; MECHANISM ; INDUCTION ; ANTIGEN ; ANTIGENS ; CELL-LINES ; CYCLE ; ASSOCIATION ; SIGNAL ; SUSCEPTIBILITY ; virus ; TRANSCRIPTION FACTORS ; OVARIAN-CANCER ; CELL-LINE ; LINE ; REPLICATION ; INTERFERON ; KINETICS ; sensitivity ; ADAPTIVE IMMUNITY ; DOUBLE-STRANDED-RNA ; BEHAVIOR ; FLUORESCENCE ; cell lines ; TUMOR CELLS ; INCREASED EXPRESSION ; RE ; INCREASE ; oncolytic virus ; ENZYME ; TUMOR-CELL ; antiviral ; ANTITUMOR VACCINATION ; antiviral proteins ; HUMAN CELL LINES ; interferon alpha ; paramyxovirus ; PROTEIN-KINASE PKR ; TRANSLATIONAL CONTROL ; virus infection
    Abstract: To investigate tumor-selective viral replication, we compared several tumorigenic human cell lines to nontumorigenic human cells from the blood for the sensitivity to become infected by a recombinant lentogenic strain of Newcastle Disease Virus (NDV) with incorporated transgene EGFP (NDFL-EGFP). Although fluorescence signals in nontumorigenic cells were only weak or missing completely, a massive and long-lasting transgene-expression was observed in all tumor cell lines. The majority of tumor cells (50-95%) could be infected, and viral replication was associated with an increase in the cell surface density of viral antigens. To clarify the underlying mechanism of the observed difference in virus susceptibility we examined the kinetics of interferon-induced antiviral enzymes because NDV is a strong type-I interferon inducer. This analysis revealed several defects of tumor cells in their antiviral defence responses: They showed no response to UV-inactivated NDV, whereas nontumorigenic cells reacted with induction of high-levels of the antiviral enzymes PKR and MxA. Upon coincubation with live NDV, tumor cells showed a delayed response in the increased expression of the antiviral enzymes in comparison with PBMC. In nontumorigenic cells the replication cycle of NDV stopped after the production of positive-strand RNA, while tumor cells continued in the replication cycle and copied viral genomes 10-50 hr after infection. These results can explain the tumor selective replication behavior of this interesting antineoplastic virus. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16470838
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  • 8
    Keywords: ANGIOGENESIS ; CANCER ; CELLS ; ENDOTHELIAL-CELLS ; GROWTH ; GROWTH-FACTOR ; IN-VITRO ; proliferation ; tumor ; carcinoma ; CELL ; CELL-PROLIFERATION ; COMBINATION ; Germany ; IN-VIVO ; MODEL ; VITRO ; VIVO ; DRUG ; MOLECULES ; NF-KAPPA-B ; MECHANISM ; treatment ; MOLECULE ; ANTITUMOR-ACTIVITY ; TARGET ; MOUSE ; INDUCED APOPTOSIS ; FIBROBLAST-GROWTH-FACTOR ; NECROSIS-FACTOR-ALPHA ; chemotherapy ; MIGRATION ; HEAD ; CARCINOMAS ; NECK ; squamous cell carcinoma ; MOUSE MODEL ; CISPLATIN ; CELL-MIGRATION ; MULTIPLE-MYELOMA ; PHASE-II ; CELL CARCINOMA ; ONCOLOGY ; tube formation ; fibroblast ; TUMOR-GROWTH ; endothelial cells ; interaction ; thalidomide ; antiangiogenic therapy ; cell proliferation ; TUMOR-CELL ; USA ; head and neck squamous cell carcinoma ; DRUGS ; vascular endothelial growth factor ; in vivo ; ENDOTHELIAL-CELL ; SQUAMOUS-CELL ; mechanism of action ; ENDOTHELIAL GROWTH ; head and neck squamous cell carcinomas ; ADVANCED MELANOMA ; DOCETAXEL TAXOTERE ; PLUS THALIDOMIDE
    Abstract: Thalidomide is an immunomodulatory, antiangiogenic drug. Although there is evidence that it might be more effective in combination with chemotherapy the exact mechanism of action is unclear. Therefore, we investigated its effect in combination with metronomically applied cisplatin in a xenotransplant mouse model characteristic for advanced head and neck squamous cell carcinomas, its possible synergistic action in vitro, and which tumor-derived factors might be targeted by thalidomide. Although thalidomide alone was ineffective, a combined treatment with low-dose cisplatin inhibited significant tumor growth, proliferation and angiogenesis in vivo as well as migration and tube formation of endothelial cells in vitro. Noteworthy, the latter effect was enhanced after coapplication of cisplatin in nontoxic doses. An inhibitory effect on tumor cell migration was also observed suggesting a direct antitumor effect. Although thalidomide alone did not influence cell proliferation, it augmented antiproliferative response after cisplatin application emphasizing the idea of a potentiated effect when both drugs are combined. Furthermore, we could show that antiangiogenic effects of thalidomide are related to tumor-cell derived factors including vascular endothelial growth factor, basic fibroblast growth factor, hepatocyte growth factor and I1-8 some known and with, granulocyte colony stimulating growth factor and granulocyte macrophage colony stimulating growth factor, some new target molecules of thalidomide. Altogether, our findings reveal new insights into thalidomide-mediated antitumor and antiangiogenic effects and its interaction with cytostatic drugs
    Type of Publication: Journal article published
    PubMed ID: 17557286
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  • 9
    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; human ; THERAPY ; VITRO ; DISEASE ; EXPOSURE ; SITE ; GENE ; PATIENT ; ACTIVATION ; IFN-GAMMA ; MARKER ; LYMPH-NODES ; T cell ; T cells ; T-CELL ; T-CELLS ; BONE-MARROW ; MEMORY ; STIMULATION ; virus ; ASSAY ; PARAMETERS ; HEAD ; VACCINE ; REPLICATION ; squamous cell carcinoma ; ELISPOT ; IMMUNOTHERAPY ; vaccination ; side effects ; IL-2 ; FUSION PROTEIN ; INTERLEUKIN-2 ; INCREASED EXPRESSION ; CELL CARCINOMA ; FEATURES ; ONCOLOGY ; RECOMBINANT ; NODES ; RE ; HNSCC ; NEWCASTLE-DISEASE-VIRUS ; Newcastle disease virus ; lymph nodes ; ANTITUMOR VACCINATION ; SQUAMOUS-CELL ; systemic ; DEGRANULATION ; cancer vaccination ; CYTOTOXIC ACTIVITY ; tumor therapy ; anti-tumor activity ; anti-tumor ; interleukin 2
    Abstract: A new recombinant (rec) Newcastle disease virus (NDV) with incorporated human interleukin 2 (IL-2) as foreign therapeutic gene [rec(IL-2)] will be described. The foreign gene in rec(IL-2) did not affect the main features of NDV replication nor its tumor selectivity. Biologically active IL-2 was produced in high amounts by tumor cells infected with rec(IL-2). Tumor vaccine cells infected by rec(IL-2) stimulated human T cells to exert anti-tumor activity in vitro in a tumor neutralization assay. These effects were significantly increased when compared to vaccine infected by rec(-) virus without IL-2 gene. After incubation with rec(IL-2) infected tumor cells, T cells showed increased expression of the activation marker CD69 and produced increased amounts of IFN gamma when compared to T cells co-incubated with rec(-) infected tumor cells. CD8 T cells incubated with rec(IL-2) infected tumor cells showed upregulation of perform, cell surface exposure of the degranulation marker CD107a and increased anti-tumor cytotoxic activity. Purified T cells from lymph nodes of head and neck squamous cell carcinoma (HNSCC) patients could be stimulated to secrete IFN gamma in an ELISPOT assay upon 40 h of stimulation with rec(IL-2) infected autologous tumor cells [ATV-rec(IL-2)] but not upon stimulation with rec(IL-2) infected allogeneic U937 tumor cells. This suggests direct activation of patient derived tumor antigen-specific memory T cells by ATV-rec(IL-2). In conclusion, the already inherent immunostimulatory properties of NDV could be further augmented by the introduction of the therapeutic gene IL-2. Active specific immunization of patients with ATV-rec(IL-2) should provide the microenvironment at the vaccination site with IL-2 and avoid side effects as seen after systemic IL-2 application
    Type of Publication: Journal article published
    PubMed ID: 18813797
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  • 10
    Keywords: CANCER ; CELLS ; SURVIVAL ; tumor ; CELL ; Germany ; THERAPY ; PATIENT ; T cells ; MUTATION ; MUTATIONS ; IMMUNOTHERAPY ; review ; THERAPIES ; cancer vaccine ; COOPERATIVE-ONCOLOGY-GROUP ; MODIFIED TUMOR-CELLS ; PROGRESSION-FREE SURVIVAL ; therapeutic ; antigen specific ; autologous ; CELL-LUNG-CANCER ; ACTIVE SPECIFIC IMMUNOTHERAPY ; allogenic ; ANTIIDIOTYPIC MONOCLONAL-ANTIBODY ; HIGH-DOSE INTERFERON-ALPHA-2B ; MELANOMA PEPTIDE VACCINE ; METASTATIC COLORECTAL-CANCER ; PHASE-II-TRIAL ; REFRACTORY PROSTATE-CANCER ; whole cell
    Abstract: This review elucidates state-of-the-art clinical studies on active specific immunotherapy with tumor vaccines. It refers solely to randomized studies and has a special focus on patient's survival, the most important parameter for any therapy. Of special interest, from a tumor immunological point of view, is a comparison between the results obtained with allogeneic tumor cell-derived vaccines and those obtained with autologous tumor cell-derived vaccines. Overall, autologous vaccines have given better results than allogeneic vaccines. Random mutations in cancer generate unique antigens in each individual case. The superiority of autologous vaccines suggests that unique tumor-associated antigens are particularly important in generating responsive T cells for a therapeutic effect
    Type of Publication: Journal article published
    PubMed ID: 19093773
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