LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Erweiterte Suche

Suchergebnis

Treffer 1 - 3 von insgesamt 3

Suchoptionen

  1. Artikel: Genetically modified T cells to target glioblastoma.

    Krebs, Simone / Rodríguez-Cruz, Tania G / Derenzo, Christopher / Gottschalk, Stephen

    Frontiers in oncology

    2013  Band 3, Seite(n) 322

    Abstract: Despite advances in surgical procedures, radiation, and chemotherapy the outcome for patients with glioblastoma (GBM) remains poor. While GBM cells express antigens that are potentially recognized by T cells, GBMs prevent the induction of GBM-specific ... ...

    Abstract Despite advances in surgical procedures, radiation, and chemotherapy the outcome for patients with glioblastoma (GBM) remains poor. While GBM cells express antigens that are potentially recognized by T cells, GBMs prevent the induction of GBM-specific immune responses by creating an immunosuppressive microenvironment. The advent of gene transfer has allowed the rapid generation of antigen-specific T cells as well as T cells with enhanced effector function. Here we review recent advances in the field of cell therapy with genetically modified T cells and how these advances might improve outcomes for patients with GBM in the future.
    Sprache Englisch
    Erscheinungsdatum 2013-12-31
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2013.00322
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  2. Artikel: Autoshaping of ethanol drinking: an animal model of binge drinking.

    Tomie, Arthur / di Poce, Jason / Derenzo, Christopher C / Pohorecky, Larissa A

    Alcohol and alcoholism (Oxford, Oxfordshire)

    2002  Band 37, Heft 2, Seite(n) 138–146

    Abstract: To examine the hypothesis that Pavlovian autoshaping provides an animal learning model of drug abuse, two studies evaluated the induction of ethanol drinking by autoshaping procedures. In Experiment 1, the sipper tube conditioned stimulus (CS) contained ... ...

    Abstract To examine the hypothesis that Pavlovian autoshaping provides an animal learning model of drug abuse, two studies evaluated the induction of ethanol drinking by autoshaping procedures. In Experiment 1, the sipper tube conditioned stimulus (CS) contained saccharin/ethanol solution and was repeatedly paired with food as an unconditioned stimulus (US). The CS-US paired group consumed more of the 0.1% saccharin-6% ethanol solution than did the CS-US random group, revealing that autoshaping conditioned responses (CR) induce ethanol drinking not attributable to pseudo-conditioning. Experiment 2 employed saccharin-fading procedures and showed that the paired vs random group differences in ethanol drinking were maintained, even as the saccharin was eliminated from the solution. The results show that Pavlovian autoshaping procedures induce high volumes of ethanol drinking when the presentation of a sipper tube containing an ethanol solution precedes the response-independent delivery of food. The high volume of ethanol consumed in a brief period of time suggests that Pavlovian autoshaping may be a model of binge drinking.
    Mesh-Begriff(e) Alcohol Drinking/psychology ; Alcoholism/psychology ; Animals ; Central Nervous System Depressants/adverse effects ; Conditioning (Psychology) ; Disease Models, Animal ; Ethanol/adverse effects ; Male ; Rats ; Rats, Long-Evans
    Chemische Substanzen Central Nervous System Depressants ; Ethanol (3K9958V90M)
    Sprache Englisch
    Erscheinungsdatum 2002-03
    Erscheinungsland England
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 604956-4
    ISSN 1464-3502 ; 0735-0414 ; 0309-1635
    ISSN (online) 1464-3502
    ISSN 0735-0414 ; 0309-1635
    DOI 10.1093/alcalc/37.2.138
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  3. Artikel ; Online: P53 regulates the migration of mesenchymal stromal cells in response to the tumor microenvironment through both CXCL12-dependent and -independent mechanisms.

    Lin, Siang-Yo / Dolfi, Sonia C / Amiri, Sohrab / Li, Jaidong / Budak-Alpdogan, Tulin / Lee, Kuo-Chieh / Derenzo, Christopher / Banerjee, Debabrata / Glod, John

    International journal of oncology

    2013  Band 43, Heft 6, Seite(n) 1817–1823

    Abstract: Mesenchymal stromal cells (MSCs) are multipotent fibroblast-like cells located in the bone marrow that localize to areas of tissue damage including wounds and solid tumors. Within the tumor microenvironment, MSCs adopt the phenotype of carcinoma- ... ...

    Abstract Mesenchymal stromal cells (MSCs) are multipotent fibroblast-like cells located in the bone marrow that localize to areas of tissue damage including wounds and solid tumors. Within the tumor microenvironment, MSCs adopt the phenotype of carcinoma-associated fibroblasts (CAFs) and stimulate tumor growth. Production of the chemokine CXCL12, also known as stromal cell-derived factor 1 (SDF-1), by MSCs is required for their in vitro migration in response to tumor cells and has also been implicated in stimulation of tumor growth. The tumor suppressor p53 regulates cellular migration, CXCL12 production and the promotion of tumor growth by carcinoma-associated fibroblasts (CAFs). We investigated the role of p53 in MSC migration to tumors. P53 inhibits the migration of MSCs in response to tumor cells in conjunction with a decrease in CXCL12 transcription. Conversely, decreased p53 activity leads to enhanced MSC migration. Interestingly, increased p53 activity inhibits MSC migration even in the context of high concentrations of exogenous CXCL12. These data show that stromal p53 status impacts the recruitment of MSCs to solid tumors through both regulation of CXCL12 production as well as other mechanisms. Stromal p53 may influence other important aspects of tumor biology such as tumor growth and metastasis through mechanisms distinct from CXCL12.
    Mesh-Begriff(e) Animals ; Cell Line, Tumor ; Cell Movement ; Chemokine CXCL12/genetics ; Chemokine CXCL12/metabolism ; Culture Media, Conditioned/pharmacology ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Humans ; Imidazoles/pharmacology ; Interleukin-8/metabolism ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Piperazines/pharmacology ; Proto-Oncogene Proteins c-mdm2/antagonists & inhibitors ; RNA Interference ; RNA, Small Interfering ; Signal Transduction ; Tumor Microenvironment ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemische Substanzen CXCL12 protein, human ; Chemokine CXCL12 ; Culture Media, Conditioned ; Cyclin-Dependent Kinase Inhibitor p21 ; Imidazoles ; Interleukin-8 ; Piperazines ; RNA, Small Interfering ; Tumor Suppressor Protein p53 ; nutlin 3 (53IA0V845C) ; Mdm2 protein, mouse (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
    Sprache Englisch
    Erscheinungsdatum 2013-09-23
    Erscheinungsland Greece
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1154403-x
    ISSN 1791-2423 ; 1019-6439
    ISSN (online) 1791-2423
    ISSN 1019-6439
    DOI 10.3892/ijo.2013.2109
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

Zum Seitenanfang