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  • 1
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; Germany ; human ; IN-VIVO ; THERAPY ; DEATH ; RISK ; PROTEIN ; DRUG ; LIGAND ; MECHANISM ; REDUCTION ; INDUCTION ; mechanisms ; DOWN-REGULATION ; treatment ; resistance ; UP-REGULATION ; sensitization ; TUMOR CELLS ; CANCER-THERAPY ; FLIP ; PPAR-GAMMA ; ACTIVATED RECEPTOR-GAMMA ; TRAIL-INDUCED APOPTOSIS ; neuroblastoma ; CASPASE ; RE ; INCREASE ; cancer therapy ; GLIOMA ; MALIGNANT GLIOMA ; brain tumors ; SURVIVIN ; LEVEL ; TUMOR-CELL ; downregulation ; AGONISTS ; APO2 LIGAND ; troglitazone
    Abstract: Induction of apoptosis by the death ligand TRAIL might be a promising therapeutic approach in cancer therapy. However, since not all tumor cells are sensitive to TRAIL, there is a need for the development of strategies to overcome TRAIL-resistance. The results of the present study show that the anti-diabetic drug troglitazone sensitizes human glioma and neuroblastoma cells to TRAIL-induced apoptosis. This process is accompanied by a substantial increase of active caspase 8 and active caspase 3, but it is independent of troglitazone's effects on the nuclear receptor PPAR-gamma. Troglitazone induces a pronounced reduction in protein expression levels of the anti-apoptotic FLICE-inhibitory protein (FLIP) without affecting FLIP mRNA levels. Further, protein and mRNA expression levels of the anti-apoptotic protein Survivin significantly decrease upon treatment with troglitazone. Moreover, sensitization to TRAIL is partly accompanied by an up-regulation of the TRAIL receptor, TRAIL-R2. A combined treatment with troglitazone and TRAIL might be a promising experimental therapy because troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via various mechanisms, thereby minimizing the risk of acquired tumor cell resistance
    Type of Publication: Journal article published
    PubMed ID: 16820965
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  • 2
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; SURVIVAL ; tumor ; Germany ; THERAPY ; DIAGNOSIS ; DISEASE ; PATIENT ; treatment ; PARTICLES ; STAGE ; REGIONS ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; TRANSLATION ; LEVEL ; cancer research ; CANCERS
    Abstract: Background: Despite great advances in basic oncology research, the situation in clinical oncology continues to be dissatisfying. Reasons for this include a lack of highly effective and specific types of treatment, late diagnosis of cancers (i.e., in advanced stages) and poor translation of new research results into clinical practice. Basic Situation: Knowledge in cancer research his grown exponentially over the past 2 decides. While our understanding of cancer development at the molecular level continues to improve, the actual transfer of these findings into practice is lagging behind today's possibilities. Examples from the German Cancer Research Center ("Deutsches Krebsforschungszentrum" [DKFZ]) and numerous other research institutes show that novel approaches in diagnostics and therapy do exist. Solution: To close the gap between basic research and clinical practice, completely new organizational forms in oncology are needed. Intelligent 0 models of integrated care of tumor patients shaped after US Comprehensive Cancer Centers may lead to fundamental improvements in clinical oncology, opening LIP a way to closely interlock research and clinical practice in order to create synergies for both sides. Such models are currently being established in different places in Germany, with the National Center for Tumor Diseases (NCT) Heidelberg occupying a special place due to its affiliation with the German Cancer Research Center. Moreover, collaboration with industry engaged in research needs to be intensified in order to advance new approaches in research to market readiness. Outlook: Cancer medicine of the future will be more specific, more individual and more interdisciplinary thin it is today. Cancer research, clinical oncology and industry engaged in research need to join forces in a strong alliance for the transfer of scientific findings into clinical application
    Type of Publication: Journal article published
    PubMed ID: 16501913
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