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  1. Artikel: Dual Role of

    Jelača, Sanja / Jovanovic, Ivan / Bovan, Dijana / Jovanovic, Marina Z / Jurisevic, Milena M / Dunđerović, Duško / Dajic-Stevanovic, Zora / Arsenijevic, Nebojsa / Mijatović, Sanja / Maksimović-Ivanić, Danijela

    Pharmaceuticals (Basel, Switzerland)

    2024  Band 17, Heft 3

    Abstract: Ethnomedicinal records have long mentioned the historical usage ... ...

    Abstract Ethnomedicinal records have long mentioned the historical usage of
    Sprache Englisch
    Erscheinungsdatum 2024-02-23
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph17030286
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Metformin promotes antitumor activity of NK cells via overexpression of miRNA-150 and miRNA-155.

    Petrovic, Andjela R / Jovanovic, Ivan P / Jurisevic, Milena M / Jovanovic, Marina Z / Jovanovic, Marina M / Pavlovic, Sladjana P / Arsenijevic, Nebojsa N / Supic, Gordana M / Vojvodic, Danilo V / Jovanovic, Milan M / Gajovic, Nevena M

    American journal of translational research

    2023  Band 15, Heft 4, Seite(n) 2727–2737

    Abstract: Objectives: Metformin, an oral anti-diabetic drug, is known to possess a powerful antitumor effect by modulating the tumor-immune interaction. The precise influence of metformin on natural killer (NK) cells, a crucial innate immunity player, is not ... ...

    Abstract Objectives: Metformin, an oral anti-diabetic drug, is known to possess a powerful antitumor effect by modulating the tumor-immune interaction. The precise influence of metformin on natural killer (NK) cells, a crucial innate immunity player, is not completely understood. In our study, analyses of the effect of metformin on the NK cell functional phenotype were performed, and the potential mechanisms underlying it were investigated.
    Methods: BALB/C wild type mice were treated with metformin, and the functional phenotype of splenocytes and potential underlying mechanisms were investigated.
    Results: Metformin significantly boosts NK cell cytotoxicity and the percentage of NKp46
    Conclusions: These findings suggest that metformin can directly potentiate NK cell activation and cytotoxicity. This research may contribute to dissecting key mechanisms of metformin exerting antitumor activity to advance the use of metformin as an antitumor agent.
    Sprache Englisch
    Erscheinungsdatum 2023-04-15
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2471058-1
    ISSN 1943-8141
    ISSN 1943-8141
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Dual blockage of PD-L/PD-1 and IL33/ST2 axes slows tumor growth and improves antitumor immunity by boosting NK cells

    Jovanovic, Marina Z. / Geller, David A. / Gajovic, Nevena M. / Jurisevic, Milena M. / Arsenijevic, Nebojsa N. / Jovanovic, Milan M. / Supic, Gordana M. / Vojvodic, Danilo V. / Jovanovic, Ivan P.

    Elsevier Inc. Life sciences. 2022 Jan. 15, v. 289

    2022  

    Abstract: Although separate blockage of either IL33/ST2 or PD-L/PD-1 axes has been shown to be beneficial in many tumors, co-blockage of IL33/ST2 and PD-L/PD-1 hasn't been studied yet.4T1 breast cancer and CT26 colon cancer were inducted in BALB/C wild type (WT) ... ...

    Abstract Although separate blockage of either IL33/ST2 or PD-L/PD-1 axes has been shown to be beneficial in many tumors, co-blockage of IL33/ST2 and PD-L/PD-1 hasn't been studied yet.4T1 breast cancer and CT26 colon cancer were inducted in BALB/C wild type (WT) and BALB/C ST2 knockout mice, after which mice underwent anti PD-1 and anti IL-33 treatment.Co-blockage of IL33/ST2 and PD-L/PD-1 delayed tumor appearance and slowed tumor growth. Enhanced NK cell cytotoxicity against 4T1 tumor cells in ST2 knockout anti-PD-1 treated mice was associated with overexpression of miRNA-150 and miRNA-155, upregulation of NFκB and STAT3, increased expression of activation markers and decreased expression of immunosuppressive markers in splenic and primary tumor derived NK cells. NK cells from ST2 knockout anti-PD-1 treated mice tend to proliferate more and are less prone to apoptosis. Accumulation of immunosuppressive myeloid derived suppressor cells and regulatory T cells was significantly impaired in spleen and primary tumor of ST2 knockout anti-PD-1 treated mice.Co-blockage of IL3/ST2 and PD-L/PD-1 axes impedes tumor progression more efficiently than single blockage of either axes, thus offering potential new approach to immunotherapy of tumors.
    Schlagwörter apoptosis ; breast neoplasms ; colorectal neoplasms ; cytotoxicity ; immunosuppression ; immunotherapy ; neoplasm progression ; spleen
    Sprache Englisch
    Erscheinungsverlauf 2022-0115
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2021.120214
    Datenquelle NAL Katalog (AGRICOLA)

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    Verfügbar in ZB MED Bonn

    Z 73/732: Hefte anzeigen

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  4. Artikel ; Online: Dual blockage of PD-L/PD-1 and IL33/ST2 axes slows tumor growth and improves antitumor immunity by boosting NK cells.

    Jovanovic, Marina Z / Geller, David A / Gajovic, Nevena M / Jurisevic, Milena M / Arsenijevic, Nebojsa N / Jovanovic, Milan M / Supic, Gordana M / Vojvodic, Danilo V / Jovanovic, Ivan P

    Life sciences

    2021  Band 289, Seite(n) 120214

    Abstract: Aims: Although separate blockage of either IL33/ST2 or PD-L/PD-1 axes has been shown to be beneficial in many tumors, co-blockage of IL33/ST2 and PD-L/PD-1 hasn't been studied yet.: Main methods: 4T1 breast cancer and CT26 colon cancer were inducted ... ...

    Abstract Aims: Although separate blockage of either IL33/ST2 or PD-L/PD-1 axes has been shown to be beneficial in many tumors, co-blockage of IL33/ST2 and PD-L/PD-1 hasn't been studied yet.
    Main methods: 4T1 breast cancer and CT26 colon cancer were inducted in BALB/C wild type (WT) and BALB/C ST2 knockout mice, after which mice underwent anti PD-1 and anti IL-33 treatment.
    Key findings: Co-blockage of IL33/ST2 and PD-L/PD-1 delayed tumor appearance and slowed tumor growth. Enhanced NK cell cytotoxicity against 4T1 tumor cells in ST2 knockout anti-PD-1 treated mice was associated with overexpression of miRNA-150 and miRNA-155, upregulation of NFκB and STAT3, increased expression of activation markers and decreased expression of immunosuppressive markers in splenic and primary tumor derived NK cells. NK cells from ST2 knockout anti-PD-1 treated mice tend to proliferate more and are less prone to apoptosis. Accumulation of immunosuppressive myeloid derived suppressor cells and regulatory T cells was significantly impaired in spleen and primary tumor of ST2 knockout anti-PD-1 treated mice.
    Significance: Co-blockage of IL3/ST2 and PD-L/PD-1 axes impedes tumor progression more efficiently than single blockage of either axes, thus offering potential new approach to immunotherapy of tumors.
    Mesh-Begriff(e) Animals ; B7-H1 Antigen/genetics ; B7-H1 Antigen/immunology ; Cell Line, Tumor ; Colonic Neoplasms/genetics ; Colonic Neoplasms/immunology ; Immunity, Cellular ; Interleukin-1 Receptor-Like 1 Protein/genetics ; Interleukin-1 Receptor-Like 1 Protein/immunology ; Interleukin-33/genetics ; Interleukin-33/immunology ; Killer Cells, Natural/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Programmed Cell Death 1 Receptor/genetics ; Programmed Cell Death 1 Receptor/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology
    Chemische Substanzen B7-H1 Antigen ; Cd274 protein, mouse ; Il1rl1 protein, mouse ; Il33 protein, mouse ; Interleukin-1 Receptor-Like 1 Protein ; Interleukin-33 ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor
    Sprache Englisch
    Erscheinungsdatum 2021-12-07
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2021.120214
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Verfügbar in ZB MED Köln/Königswinter

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