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  1. Book ; Online: The Role of Complement in Tumors

    Rolfe, Barbara / Pio, Ruben / Woodruff, Trent M. / Markiewski, Maciej M. / Manthey, Helga D.

    2020  

    Keywords Medicine ; Immunology ; complement ; cancer ; metastasis ; C5b-9 ; C1q ; C3a ; C5a ; complement regulatory proteins
    Size 1 electronic resource (107 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230763
    ISBN 9782889635764 ; 2889635767
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Inside-Out of Complement in Cancer.

    Kolev, Martin / Das, Madhumita / Gerber, Monica / Baver, Scott / Deschatelets, Pascal / Markiewski, Maciej M

    Frontiers in immunology

    2022  Volume 13, Page(s) 931273

    Abstract: The role of complement in cancer has received increasing attention over the last decade. Recent studies provide compelling evidence that complement accelerates cancer progression. Despite the pivotal role of complement in fighting microbes, complement ... ...

    Abstract The role of complement in cancer has received increasing attention over the last decade. Recent studies provide compelling evidence that complement accelerates cancer progression. Despite the pivotal role of complement in fighting microbes, complement seems to suppress antitumor immunity
    MeSH term(s) Complement Activation ; Complement System Proteins ; Humans ; Neoplasms ; T-Lymphocytes ; Tumor Microenvironment
    Chemical Substances Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2022-07-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.931273
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Targeting complement-mediated immunoregulation for cancer immunotherapy.

    Kolev, Martin / Markiewski, Maciej M

    Seminars in immunology

    2018  Volume 37, Page(s) 85–97

    Abstract: Complement was initially discovered as an assembly of plasma proteins "complementing" the cytolytic activity of antibodies. However, our current knowledge places this complex system of several plasma proteins, receptors, and regulators in the center of ... ...

    Abstract Complement was initially discovered as an assembly of plasma proteins "complementing" the cytolytic activity of antibodies. However, our current knowledge places this complex system of several plasma proteins, receptors, and regulators in the center of innate immunity as a bridge between the initial innate responses and adaptive immune reactions. Consequently, complement appears to be pivotal for elimination of pathogens, not only as an early response defense, but by directing the subsequent adaptive immune response. The discovery of functional intracellular complement and its roles in cellular metabolism opened novel avenues for research and potential therapeutic implications. The recent studies demonstrating immunoregulatory functions of complement in the tumor microenvironment and the premetastatic niche shifted the paradigm on our understanding of functions of the complement system in regulating immunity. Several complement proteins, through their interaction with cells in the tumor microenvironment and in metastasis-targeted organs, contribute to modulating tumor growth, antitumor immunity, angiogenesis, and therefore, the overall progression of malignancy and, perhaps, responsiveness of cancer to different therapies. Here, we focus on recent progress in our understanding of immunostimulatory vs. immunoregulatory functions of complement and potential applications of these findings to the design of novel therapies for cancer patients.
    MeSH term(s) Animals ; Complement Activation ; Complement System Proteins/metabolism ; Cytotoxicity, Immunologic ; Humans ; Immunity, Innate ; Immunomodulation ; Immunotherapy/methods ; Neoplasms/immunology ; Neoplasms/therapy ; Tumor Microenvironment
    Chemical Substances Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2018-02-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1018141-6
    ISSN 1096-3618 ; 1044-5323
    ISSN (online) 1096-3618
    ISSN 1044-5323
    DOI 10.1016/j.smim.2018.02.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2843: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Nanoparticle-Induced Complement Activation: Implications for Cancer Nanomedicine.

    La-Beck, Ninh M / Islam, Md Rakibul / Markiewski, Maciej M

    Frontiers in immunology

    2021  Volume 11, Page(s) 603039

    Abstract: Nanoparticle-based anticancer medications were first approved for cancer treatment almost 2 decades ago. Patients benefit from these approaches because of the targeted-drug delivery and reduced toxicity, however, like other therapies, adverse reactions ... ...

    Abstract Nanoparticle-based anticancer medications were first approved for cancer treatment almost 2 decades ago. Patients benefit from these approaches because of the targeted-drug delivery and reduced toxicity, however, like other therapies, adverse reactions often limit their use. These reactions are linked to the interactions of nanoparticles with the immune system, including the activation of complement. This activation can cause well-characterized acute inflammatory reactions mediated by complement effectors. However, the long-term implications of chronic complement activation on the efficacy of drugs carried by nanoparticles remain obscured. The recent discovery of protumor roles of complement raises the possibility that nanoparticle-induced complement activation may actually reduce antitumor efficacy of drugs carried by nanoparticles. We discuss here the initial evidence supporting this notion. Better understanding of the complex interactions between nanoparticles, complement, and the tumor microenvironment appears to be critical for development of nanoparticle-based anticancer therapies that are safer and more efficacious.
    MeSH term(s) Animals ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/chemistry ; Complement Activation/drug effects ; Drug Carriers/adverse effects ; Drug Compounding ; Humans ; Nanomedicine ; Nanoparticles/adverse effects ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Tumor Microenvironment
    Chemical Substances Antineoplastic Agents ; Drug Carriers
    Language English
    Publishing date 2021-01-08
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.603039
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Role of Complement in Angiogenesis.

    Markiewski, Maciej M / Daugherity, Elizabeth / Reese, Britney / Karbowniczek, Magdalena

    Antibodies (Basel, Switzerland)

    2020  Volume 9, Issue 4

    Abstract: The link of the complement system to angiogenesis has remained circumstantial and speculative for several years. Perhaps the most clinically relevant example of possible involvement of complement in pathological neovascularization is age-related macular ... ...

    Abstract The link of the complement system to angiogenesis has remained circumstantial and speculative for several years. Perhaps the most clinically relevant example of possible involvement of complement in pathological neovascularization is age-related macular degeneration. Recent studies, however, provide more direct and experimental evidence that indeed the complement system regulates physiological and pathological angiogenesis in models of wound healing, retinal regeneration, age-related macular degeneration, and cancer. Interestingly, complement-dependent mechanisms involved in angiogenesis are very much context dependent, including anti- and proangiogenic functions. Here, we discuss these new developments that place complement among other important regulators of homeostatic and pathological angiogenesis, and we provide the perspective on how these newly discovered complement functions can be targeted for therapy.
    Language English
    Publishing date 2020-12-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 2073-4468
    ISSN (online) 2073-4468
    DOI 10.3390/antib9040067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Listeria-based immunotherapy directed against CD105 exerts anti-angiogenic and anti-tumor efficacy in renal cell carcinoma.

    Oladejo, Mariam / Nguyen, Hong-My / Silwal, Ashok / Reese, Britney / Paulishak, Wyatt / Markiewski, Maciej M / Wood, Laurence M

    Frontiers in immunology

    2022  Volume 13, Page(s) 1038807

    Abstract: Targeting tumor-associated angiogenesis is currently at the forefront of renal cell carcinoma (RCC) therapy, with sunitinib and bevacizumab leading to increased survival in patients with metastatic RCC (mRCC). However, resistance often occurs shortly ... ...

    Abstract Targeting tumor-associated angiogenesis is currently at the forefront of renal cell carcinoma (RCC) therapy, with sunitinib and bevacizumab leading to increased survival in patients with metastatic RCC (mRCC). However, resistance often occurs shortly after initiation of therapy, suggesting that targeting the tumor-associated vascular endothelium may not be sufficient to eradicate RCC. This study reports the therapeutic efficacy of a Listeria (Lm)-based vaccine encoding an antigenic fragment of CD105 (Lm-LLO-CD105A) that targets both RCC tumor cells and the tumor-associated vasculature. Lm-LLO-CD105A treatment reduced primary tumor growth in both subcutaneous and orthotopic models of murine RCC. The vaccine conferred anti-tumor immunity and remodeled the tumor microenvironment (TME), resulting in increased infiltration of polyfunctional CD8
    MeSH term(s) Humans ; Mice ; Animals ; Carcinoma, Renal Cell/drug therapy ; Listeria ; CD8-Positive T-Lymphocytes ; Cancer Vaccines ; Cell Line, Tumor ; Immunotherapy/methods ; Neovascularization, Pathologic/drug therapy ; Kidney Neoplasms/pathology ; Tumor Microenvironment
    Chemical Substances Cancer Vaccines
    Language English
    Publishing date 2022-11-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1038807
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Atovaquone Suppresses Triple-Negative Breast Tumor Growth by Reducing Immune-Suppressive Cells.

    Gupta, Nehal / Gaikwad, Shreyas / Kaushik, Itishree / Wright, Stephen E / Markiewski, Maciej M / Srivastava, Sanjay K

    International journal of molecular sciences

    2021  Volume 22, Issue 10

    Abstract: A major contributing factor in triple-negative breast cancer progression is its ability to evade immune surveillance. One mechanism for this immunosuppression is through ribosomal protein S19 (RPS19), which facilitates myeloid-derived suppressor cells ( ... ...

    Abstract A major contributing factor in triple-negative breast cancer progression is its ability to evade immune surveillance. One mechanism for this immunosuppression is through ribosomal protein S19 (RPS19), which facilitates myeloid-derived suppressor cells (MDSCs) recruitment in tumors, which generate cytokines TGF-β and IL-10 and induce regulatory T cells (Tregs), all of which are immunosuppressive and enhance tumor progression. Hence, enhancing the immune system in breast tumors could be a strategy for anticancer therapeutics. The present study evaluated the immune response of atovaquone, an antiprotozoal drug, in three independent breast-tumor models. Our results demonstrated that oral administration of atovaquone reduced HCC1806, CI66 and 4T1 paclitaxel-resistant (4T1-PR) breast-tumor growth by 45%, 70% and 42%, respectively. MDSCs, TGF-β, IL-10 and Tregs of blood and tumors were analyzed from all of these in vivo models. Our results demonstrated that atovaquone treatment in mice bearing HCC1806 tumors reduced MDSCs from tumor and blood by 70% and 30%, respectively. We also observed a 25% reduction in tumor MDSCs in atovaquone-treated mice bearing CI66 and 4T1-PR tumors. In addition, a decrease in TGF-β and IL-10 in tumor lysates was observed in atovaquone-treated mice with a reduction in tumor Tregs. Moreover, a significant reduction in the expression of RPS19 was found in tumors treated with atovaquone.
    MeSH term(s) Animals ; Anti-Infective Agents/pharmacology ; Antigen Presentation/immunology ; Apoptosis ; Atovaquone/pharmacology ; Cell Proliferation ; Cytokines/metabolism ; Female ; Humans ; Immunosuppression Therapy ; Mice ; Mice, Inbred BALB C ; Mice, Inbred NOD ; Mice, SCID ; Myeloid-Derived Suppressor Cells/drug effects ; Myeloid-Derived Suppressor Cells/immunology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
    Chemical Substances Anti-Infective Agents ; Cytokines ; Atovaquone (Y883P1Z2LT)
    Language English
    Publishing date 2021-05-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22105150
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Editorial: The Role of Complement in Tumors.

    Rolfe, Barbara E / Pio, Ruben / Woodruff, Trent M / Markiewski, Maciej M / Manthey, Helga D

    Frontiers in immunology

    2020  Volume 11, Page(s) 139

    MeSH term(s) Animals ; Complement Activation/drug effects ; Complement System Proteins/immunology ; Cytotoxicity, Immunologic ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Immunotherapy/methods ; Molecular Targeted Therapy/methods ; Neoplasms/drug therapy ; Neoplasms/immunology
    Chemical Substances Immune Checkpoint Inhibitors ; Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2020-02-11
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.00139
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Pegylated Liposomal Alendronate Biodistribution, Immune Modulation, and Tumor Growth Inhibition in a Murine Melanoma Model.

    Islam, Md Rakibul / Patel, Jalpa / Back, Patricia Ines / Shmeeda, Hilary / Kallem, Raja Reddy / Shudde, Claire / Markiewski, Maciej / Putnam, William C / Gabizon, Alberto A / La-Beck, Ninh M

    Biomolecules

    2023  Volume 13, Issue 9

    Abstract: While tumor-associated macrophages (TAM) have pro-tumoral activity, the ablation of macrophages in cancer may be undesirable since they also have anti-tumoral functions, including T cell priming and activation against tumor antigens. Alendronate is a ... ...

    Abstract While tumor-associated macrophages (TAM) have pro-tumoral activity, the ablation of macrophages in cancer may be undesirable since they also have anti-tumoral functions, including T cell priming and activation against tumor antigens. Alendronate is a potent amino-bisphosphonate that modulates the function of macrophages in vitro, with potential as an immunotherapy if its low systemic bioavailability can be addressed. We repurposed alendronate in a non-leaky and long-circulating liposomal carrier similar to that of the clinically approved pegylated liposomal doxorubicin to facilitate rapid clinical translation. Here, we tested liposomal alendronate (PLA) as an immunotherapeutic agent for cancer in comparison with a standard of care immunotherapy, a PD-1 immune checkpoint inhibitor. We showed that the PLA induced bone marrow-derived murine non-activated macrophages and M2-macrophages to polarize towards an M1-functionality, as evidenced by gene expression, cytokine secretion, and lipidomic profiles. Free alendronate had negligible effects, indicating that liposome encapsulation is necessary for the modulation of macrophage activity. In vivo, the PLA showed significant accumulation in tumor and tumor-draining lymph nodes, sites of tumor immunosuppression that are targets of immunotherapy. The PLA remodeled the tumor microenvironment towards a less immunosuppressive milieu, as indicated by a decrease in TAM and helper T cells, and inhibited the growth of established tumors in the B16-OVA melanoma model. The improved bioavailability and the beneficial effects of PLA on macrophages suggest its potential application as immunotherapy that could synergize with T-cell-targeted therapies and chemotherapies to induce immunogenic cell death. PLA warrants further clinical development, and these clinical trials should incorporate tumor and blood biomarkers or immunophenotyping studies to verify the anti-immunosuppressive effect of PLA in humans.
    Language English
    Publishing date 2023-08-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom13091309
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Single-cell multiomic analysis identifies a HOX-PBX gene network regulating the survival of lymphangioleiomyomatosis cells.

    Olatoke, Tasnim / Wagner, Andrew / Astrinidis, Aristotelis / Zhang, Erik Y / Guo, Minzhe / Zhang, Alan G / Mattam, Ushodaya / Kopras, Elizabeth J / Gupta, Nishant / Smith, Eric P / Karbowniczek, Magdalena / Markiewski, Maciej M / Wikenheiser-Brokamp, Kathryn A / Whitsett, Jeffrey A / McCormack, Francis X / Xu, Yan / Yu, Jane J

    Science advances

    2023  Volume 9, Issue 19, Page(s) eadf8549

    Abstract: Lymphangioleiomyomatosis (LAM) is a rare, progressive lung disease that predominantly affects women. LAM cells ... ...

    Abstract Lymphangioleiomyomatosis (LAM) is a rare, progressive lung disease that predominantly affects women. LAM cells carry
    MeSH term(s) Humans ; Single-Cell Analysis ; Lymphangioleiomyomatosis/metabolism ; Lymphangioleiomyomatosis/pathology ; Gene Regulatory Networks ; Homeodomain Proteins ; Transcription Factors/metabolism ; Lung/metabolism ; Lung/pathology ; Animals ; Rats ; Neoplasm Metastasis ; Multiomics ; Female
    Chemical Substances Homeodomain Proteins ; Transcription Factors
    Language English
    Publishing date 2023-05-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adf8549
    Database MEDical Literature Analysis and Retrieval System OnLINE

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