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  1. Book ; Online ; E-Book: Tumor immune microenvironment in cancer progression and cancer therapy

    Kalinski, Pawel

    (Advances in experimental medicine and biology ; 1036)

    2017  

    Author's details Pawel Kalinski editor
    Series title Advances in experimental medicine and biology ; 1036
    Collection
    Keywords Medicine ; Cancer research ; Immunology ; Molecular biology ; Oncology ; Biomedicine
    Language English
    Size 1 Online-Ressource (xiv, 264 Seiten), Illustrationen
    Publisher Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT019555868
    ISBN 978-3-319-67577-0 ; 9783319675756 ; 3-319-67577-X ; 3319675753
    DOI 10.1007/978-3-319-67577-0
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Tumor immune microenvironment in cancer progression and cancer therapy

    Kalinski, Pawel

    (Advances in experimental medicine and biology ; 1036)

    2017  

    Author's details Pawel Kalinski editor
    Series title Advances in experimental medicine and biology ; 1036
    Collection
    Keywords Medicine ; Cancer research ; Immunology ; Molecular biology ; Oncology ; Biomedicine
    Language English
    Size XIV, 264 Seiten, Illustrationen
    Publisher Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT019555888
    ISBN 978-3-319-67575-6 ; 3-319-67575-3
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 3192 -1036- not available for loan Zeitschriften-Lesesaal

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  3. Article ; Online: Breaking Barriers: Modulation of Tumor Microenvironment to Enhance Bacillus Calmette-Guérin Immunotherapy of Bladder Cancer.

    Ibrahim, Omar M / Kalinski, Pawel

    Cells

    2024  Volume 13, Issue 8

    Abstract: The clinical management of bladder cancer continues to present significant challenges. Bacillus Calmette-Guérin (BCG) immunotherapy remains the gold standard of treatment for non-muscle invasive bladder cancer (NMIBC), but many patients develop ... ...

    Abstract The clinical management of bladder cancer continues to present significant challenges. Bacillus Calmette-Guérin (BCG) immunotherapy remains the gold standard of treatment for non-muscle invasive bladder cancer (NMIBC), but many patients develop recurrence and progression to muscle-invasive disease (MIBC), which is resistant to BCG. This review focuses on the immune mechanisms mobilized by BCG in bladder cancer tumor microenvironments (TME), mechanisms of BCG resistance, the dual role of the BCG-triggered NFkB/TNFα/PGE2 axis in the regulation of anti-tumor and tumor-promoting aspects of inflammation, and emerging strategies to modulate their balance. A better understanding of BCG resistance will help develop new treatments and predictive biomarkers, paving the way for improved clinical outcomes in bladder cancer patients.
    MeSH term(s) Urinary Bladder Neoplasms/immunology ; Urinary Bladder Neoplasms/therapy ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/pathology ; Humans ; Tumor Microenvironment/immunology ; BCG Vaccine/therapeutic use ; BCG Vaccine/immunology ; Immunotherapy/methods ; Animals
    Chemical Substances BCG Vaccine
    Language English
    Publishing date 2024-04-18
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells13080699
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Cytotoxic T-lymphocyte infiltration and chemokine predict long-term patient survival independently of tumor mutational burden in triple-negative breast cancer.

    Katsuta, Eriko / Yan, Li / Opyrchal, Mateusz / Kalinski, Pawel / Takabe, Kazuaki

    Therapeutic advances in medical oncology

    2021  Volume 13, Page(s) 17588359211006680

    Abstract: Background: Cytotoxic T-lymphocyte (CTL) infiltration into tumor is a positive prognostic factor in breast cancer. High tumor mutational burden (TMB) is also considered as a predictor of tumor immunogenicity and response to immunotherapy. However, it is ...

    Abstract Background: Cytotoxic T-lymphocyte (CTL) infiltration into tumor is a positive prognostic factor in breast cancer. High tumor mutational burden (TMB) is also considered as a predictor of tumor immunogenicity and response to immunotherapy. However, it is unclear whether the infiltration of functional CTL simply reflects the TMB or represents an independent prognostic value.
    Methods: Utilizing The Cancer Genome Atlas (TCGA) breast cancer cohort, we established the Functional Hotness Score (FHS). The associations of FHS and breast cancer patient prognosis as well as distinct immunity markers were analyzed in a total of 3011 breast cancer patients using TCGA, METABRIC and metastatic breast cancer (MBC) cohort GSE110590.
    Results: We established FHS, based on
    Conclusion: TNBCs with high FHS based on the expression levels of
    Language English
    Publishing date 2021-04-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 2503443-1
    ISSN 1758-8359 ; 1758-8340
    ISSN (online) 1758-8359
    ISSN 1758-8340
    DOI 10.1177/17588359211006680
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Antagonism of regulatory ISGs enhances the anti-melanoma efficacy of STING agonists.

    Filderman, Jessica N / Taylor, Jennifer L / Wang, Jianmin / Zhang, Yali / Singh, Prashant / Ross, Mark A / Watkins, Simon C / Nedal Al Bzour, Ayah / Karapetyan, Lilit / Kalinski, Pawel / Storkus, Walter J

    Frontiers in immunology

    2024  Volume 15, Page(s) 1334769

    Abstract: Background: Stimulator of Interferon Genes (STING) is a dsDNA sensor that triggers type I inflammatory responses. Recent data from our group and others support the therapeutic efficacy of STING agonists applied intratumorally or systemically in a range ... ...

    Abstract Background: Stimulator of Interferon Genes (STING) is a dsDNA sensor that triggers type I inflammatory responses. Recent data from our group and others support the therapeutic efficacy of STING agonists applied intratumorally or systemically in a range of murine tumor models, with treatment benefits associated with tumor vascular normalization and improved immune cell recruitment and function within the tumor microenvironment (TME). However, such interventions are rarely curative and STING agonism coordinately upregulates expression of immunoregulatory interferon-stimulated genes (ISGs) including
    Methods: Mice bearing either B16 (BRAF
    Results: In the B16 melanoma model, we noted improved antitumor efficacy only when ADU-S100 was combined with neutralizing/blocking antibodies against PD-L1 or ISG15, but not inhibitors of ARG2, COX2, or NOS2. Conversely, in the BPR20 melanoma model, improved tumor growth control vs. ADU-S100 monotherapy was only observed when combining ADU-S100 with ARG2i, COX2i, and NOS2i, but not anti-PD-L1 or anti-ISG15. Immune changes in the TME associated with improved treatment outcomes were subtle but included increases in proinflammatory innate immune cells and activated CD8
    Conclusions: These data suggest contextual differences in the relative contributions of individual regulatory ISGs that serve to operationally limit the anti-tumor efficacy of STING agonists which should be considered in future design of novel combination protocols for optimal treatment benefit.
    MeSH term(s) Mice ; Animals ; B7-H1 Antigen ; Proto-Oncogene Proteins B-raf ; Cyclooxygenase 2 ; Cell Line, Tumor ; Melanoma, Experimental ; Interferons ; Tumor Microenvironment
    Chemical Substances B7-H1 Antigen ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Interferons (9008-11-1)
    Language English
    Publishing date 2024-01-18
    Publishing country Switzerland
    Document type 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.2024.1334769
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Role of tumor microenvironment in the efficacy of BCG therapy.

    Ibrahim, Omar M / Pandey, Ravindra K / Chatta, Gurkamal / Kalinski, Pawel

    Trends in research

    2020  Volume 3, Issue 4

    Abstract: Despite its significant overall efficacy, BCG fails to benefit a substantial proportion of bladder cancer (BlCa) patients. Here, we review recent data highlighting the role of tumor microenvironment (TME) in limiting antitumoral activity of BCG treatment ...

    Abstract Despite its significant overall efficacy, BCG fails to benefit a substantial proportion of bladder cancer (BlCa) patients. Here, we review recent data highlighting the role of tumor microenvironment (TME) in limiting antitumoral activity of BCG treatment and emerging opportunities to target TME to enhance the overall outcomes in BCG-treated BlCa patients.
    Language English
    Publishing date 2020-08-17
    Publishing country England
    Document type Journal Article
    ISSN 2516-7138
    ISSN (online) 2516-7138
    DOI 10.15761/tr.1000170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Role of the DEAD-box RNA helicase DDX5 (p68) in cancer DNA repair, immune suppression, cancer metabolic control, virus infection promotion, and human microbiome (microbiota) negative influence.

    Li, Fengzhi / Ling, Xiang / Chakraborty, Sayan / Fountzilas, Christos / Wang, Jianmin / Jamroze, Anmbreen / Liu, Xiaozhuo / Kalinski, Pawel / Tang, Dean G

    Journal of experimental & clinical cancer research : CR

    2023  Volume 42, Issue 1, Page(s) 213

    Abstract: There is increasing evidence indicating the significant role of DDX5 (also called p68), acting as a master regulator and a potential biomarker and target, in tumorigenesis, proliferation, metastasis and treatment resistance for cancer therapy. However, ... ...

    Abstract There is increasing evidence indicating the significant role of DDX5 (also called p68), acting as a master regulator and a potential biomarker and target, in tumorigenesis, proliferation, metastasis and treatment resistance for cancer therapy. However, DDX5 has also been reported to act as an oncosuppressor. These seemingly contradictory observations can be reconciled by DDX5's role in DNA repair. This is because cancer cell apoptosis and malignant transformation can represent the two possible outcomes of a single process regulated by DDX5, reflecting different intensity of DNA damage. Thus, targeting DDX5 could potentially shift cancer cells from a growth-arrested state (necessary for DNA repair) to apoptosis and cell killing. In addition to the increasingly recognized role of DDX5 in global genome stability surveillance and DNA damage repair, DDX5 has been implicated in multiple oncogenic signaling pathways. DDX5 appears to utilize distinct signaling cascades via interactions with unique proteins in different types of tissues/cells to elicit opposing roles (e.g., smooth muscle cells versus cancer cells). Such unique features make DDX5 an intriguing therapeutic target for the treatment of human cancers, with limited low toxicity to normal tissues. In this review, we discuss the multifaceted functions of DDX5 in DNA repair in cancer, immune suppression, oncogenic metabolic rewiring, virus infection promotion, and negative impact on the human microbiome (microbiota). We also provide new data showing that FL118, a molecular glue DDX5 degrader, selectively works against current treatment-resistant prostate cancer organoids/cells. Altogether, current studies demonstrate that DDX5 may represent a unique oncotarget for effectively conquering cancer with minimal toxicity to normal tissues.
    MeSH term(s) Humans ; Male ; Cell Transformation, Neoplastic ; DEAD-box RNA Helicases/genetics ; DNA Repair ; Microbiota ; Prostatic Neoplasms ; Signal Transduction ; Immunosuppression Therapy
    Chemical Substances DEAD-box RNA Helicases (EC 3.6.4.13) ; Ddx5 protein, human (EC 3.6.1.-)
    Language English
    Publishing date 2023-08-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-023-02787-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  8. Article ; Online: Regulation of immune responses by prostaglandin E2.

    Kalinski, Pawel

    Journal of immunology (Baltimore, Md. : 1950)

    2011  Volume 188, Issue 1, Page(s) 21–28

    Abstract: PGE(2), an essential homeostatic factor, is also a key mediator of immunopathology in chronic infections and cancer. The impact of PGE(2) reflects the balance between its cyclooxygenase 2-regulated synthesis and 15-hydroxyprostaglandin dehydrogenase- ... ...

    Abstract PGE(2), an essential homeostatic factor, is also a key mediator of immunopathology in chronic infections and cancer. The impact of PGE(2) reflects the balance between its cyclooxygenase 2-regulated synthesis and 15-hydroxyprostaglandin dehydrogenase-driven degradation and the pattern of expression of PGE(2) receptors. PGE(2) enhances its own production but suppresses acute inflammatory mediators, resulting in its predominance at late/chronic stages of immunity. PGE(2) supports activation of dendritic cells but suppresses their ability to attract naive, memory, and effector T cells. PGE(2) selectively suppresses effector functions of macrophages and neutrophils and the Th1-, CTL-, and NK cell-mediated type 1 immunity, but it promotes Th2, Th17, and regulatory T cell responses. PGE(2) modulates chemokine production, inhibiting the attraction of proinflammatory cells while enhancing local accumulation of regulatory T cells cells and myeloid-derived suppressor cells. Targeting the production, degradation, and responsiveness to PGE(2) provides tools to modulate the patterns of immunity in a wide range of diseases, from autoimmunity to cancer.
    MeSH term(s) Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Chemokines/immunology ; Chemokines/metabolism ; Cyclooxygenase 2/immunology ; Cyclooxygenase 2/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Dinoprostone/immunology ; Dinoprostone/metabolism ; Humans ; Immunologic Memory/physiology ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Neoplasms/immunology ; Neoplasms/metabolism
    Chemical Substances Chemokines ; Inflammation Mediators ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2011-12-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1101029
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.37: Show issues Location:
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  9. Article: NK Receptors Replace CD28 As the Dominant Source of Signal 2 for Cognate Recognition of Cancer Cells by TAA-specific Effector CD8

    Dong, Bowen / Obermajer, Nataša / Tsuji, Takemasa / Matsuzaki, Junko / Bonura, Cindy / Withers, Henry / Long, Mark / Chavel, Colin / Olejniczak, Scott H / Minderman, Hans / Edwards, Robert P / Storkus, Walter J / Romero, Pedro / Kalinski, Pawel

    Research square

    2023  

    Abstract: CD28-driven "signal 2" is critical for naïve ... ...

    Abstract CD28-driven "signal 2" is critical for naïve CD8
    Language English
    Publishing date 2023-10-19
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3399211/v1
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  10. Article: Tumor Immuno-Environment in Cancer Progression and Therapy.

    Kalinski, Pawel / Talmadge, James E

    Advances in experimental medicine and biology

    2017  Volume 1036, Page(s) 1–18

    Abstract: The approvals of Provenge (Sipuleucel-T), Ipilimumab (Yervoy/anti-CTLA-4) and blockers of the PD-1 - PD-L1/PD-L2 pathway, such as nivolumab (Opdivo), pembrolizumab (Keytruda), or atezolizumab (Tecentriq), have established immunotherapy as a key component ...

    Abstract The approvals of Provenge (Sipuleucel-T), Ipilimumab (Yervoy/anti-CTLA-4) and blockers of the PD-1 - PD-L1/PD-L2 pathway, such as nivolumab (Opdivo), pembrolizumab (Keytruda), or atezolizumab (Tecentriq), have established immunotherapy as a key component of comprehensive cancer care. Further, murine mechanistic studies and studies in immunocompromised patients have documented the critical role of immunity in effectiveness of radio- and chemotherapy. However, in addition to the ability of the immune system to control cancer progression, it can also promote tumor growth, via regulatory T cells (Tregs), myeloid-derived dendritic cells (MDSCs) and tumor associated macrophages (TAM), which can enhance survival of cancer cells directly or via the regulation of the tumor stroma.An increasing body of evidence supports a central role for the tumor microenvironment (TME) and the interactions between tumor stroma, infiltrating immune cells and cancer cells during the induction and effector phase of anti-cancer immunity, and the overall effectiveness of immunotherapy and other forms of cancer treatment. In this chapter, we discuss the roles of key TME components during tumor progression, metastatic process and cancer therapy-induced tumor regression, as well as opportunities for their modulation to enhance the overall therapeutic benefit.
    MeSH term(s) Animals ; Humans ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Tumor Microenvironment/immunology
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Introductory Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-3-319-67577-0_1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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