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  1. Article ; Online: Inflammation: the incubator of the tumor microenvironment.

    Denk, Dominic / Greten, Florian R

    Trends in cancer

    2022  Volume 8, Issue 11, Page(s) 901–914

    Abstract: An inflammatory microenvironment, either conferred by an underlying chronic overt or smoldering inflammatory condition constitutes a prerequisite and fuel to essentially all cancers. The complex reciprocal interplay of different cell types in the tumor ... ...

    Abstract An inflammatory microenvironment, either conferred by an underlying chronic overt or smoldering inflammatory condition constitutes a prerequisite and fuel to essentially all cancers. The complex reciprocal interplay of different cell types in the tumor microenvironment (TME) determines patient outcome. Apart from the actual tumor cells, local and recruited nonmalignant cells as well as the intestinal microbiome actively shape polarization and plasticity of cells in the TME, thereby augmenting protumorigenic and prometastatic inflammatory processes. Here, we address the universality of inflammation in carcinogenesis, review distinct forms of tumor related inflammation and highlight critical processes in the TME actively sustaining a nurturing incubator for cancer progression and therapy resistance.
    MeSH term(s) Humans ; Tumor Microenvironment ; Carcinogenesis/metabolism ; Neoplasms/pathology ; Inflammation ; Incubators
    Language English
    Publishing date 2022-07-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2022.07.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Immune cell - produced ROS and their impact on tumor growth and metastasis.

    Kennel, Kilian B / Greten, Florian R

    Redox biology

    2021  Volume 42, Page(s) 101891

    Abstract: Reactive oxygen species (ROS) are derivatives of molecular oxygen ( ... ...

    Abstract Reactive oxygen species (ROS) are derivatives of molecular oxygen (O
    MeSH term(s) Humans ; Immune Tolerance ; Immunotherapy ; Neoplasms/therapy ; Reactive Oxygen Species ; Tumor Microenvironment
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2021-02-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2021.101891
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The inflammatory pathogenesis of colorectal cancer.

    Schmitt, Mark / Greten, Florian R

    Nature reviews. Immunology

    2021  Volume 21, Issue 10, Page(s) 653–667

    Abstract: The mutational landscape of colorectal cancer (CRC) does not enable predictions to be made about the survival of patients or their response to therapy. Instead, studying the polarization and activation profiles of immune cells and stromal cells in the ... ...

    Abstract The mutational landscape of colorectal cancer (CRC) does not enable predictions to be made about the survival of patients or their response to therapy. Instead, studying the polarization and activation profiles of immune cells and stromal cells in the tumour microenvironment has been shown to be more informative, thus making CRC a prototypical example of the importance of an inflammatory microenvironment for tumorigenesis. Here, we review our current understanding of how colon cancer cells interact with their microenvironment, comprised of immune cells, stromal cells and the intestinal microbiome, to suppress or escape immune responses and how inflammatory processes shape the immune pathogenesis of CRC.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic ; Colorectal Neoplasms/complications ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/pathology ; Gastrointestinal Microbiome ; Humans ; Inflammation/complications ; Inflammation/immunology ; Inflammation/pathology ; Stromal Cells ; Tumor Microenvironment
    Language English
    Publishing date 2021-04-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-021-00534-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Cancer: Tumour stem-cell surprises.

    Greten, Florian R

    Nature

    2017  Volume 543, Issue 7647, Page(s) 626–627

    MeSH term(s) Humans ; Neoplasms ; Neoplastic Stem Cells
    Language English
    Publishing date 2017--29
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/543626a
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Irony of Tumor-Induced Inflammation.

    Greten, Florian R

    Cell metabolism

    2016  Volume 24, Issue 3, Page(s) 368–369

    Abstract: Increased dietary iron intake and elevated systemic iron levels are associated with increased cancer risk. In this issue, Xue et al. (2016) have identified an unexpected link between intracellular iron accumulation and pro-inflammatory signaling that ... ...

    Abstract Increased dietary iron intake and elevated systemic iron levels are associated with increased cancer risk. In this issue, Xue et al. (2016) have identified an unexpected link between intracellular iron accumulation and pro-inflammatory signaling that provides, at least in part, a molecular explanation for the tumor-promoting effects of iron.
    MeSH term(s) Diet ; Humans ; Inflammation ; Iron ; Iron, Dietary ; Neoplasms
    Chemical Substances Iron, Dietary ; Iron (E1UOL152H7)
    Language English
    Publishing date 2016-09-13
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2016.08.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Inflammation and Cancer: Triggers, Mechanisms, and Consequences.

    Greten, Florian R / Grivennikov, Sergei I

    Immunity

    2019  Volume 51, Issue 1, Page(s) 27–41

    Abstract: Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells, as well as surrounding stromal and inflammatory cells, engage in well-orchestrated reciprocal interactions to form an inflammatory tumor ... ...

    Abstract Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells, as well as surrounding stromal and inflammatory cells, engage in well-orchestrated reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cells within the TME are highly plastic, continuously changing their phenotypic and functional characteristics. Here, we review the origins of inflammation in tumors, and the mechanisms whereby inflammation drives tumor initiation, growth, progression, and metastasis. We discuss how tumor-promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis, or tissue repair and illuminate the distinctions between tissue-protective and pro-tumorigenic inflammation, including spatiotemporal considerations. Defining the cornerstone rules of engagement governing molecular and cellular mechanisms of tumor-promoting inflammation will be essential for further development of anti-cancer therapies.
    MeSH term(s) Animals ; Autoimmunity ; Carcinogenesis ; Chronic Disease ; Homeostasis ; Humans ; Infections/immunology ; Inflammation ; Neoplasms/immunology ; Neovascularization, Pathologic ; Tumor Microenvironment ; Wound Healing
    Language English
    Publishing date 2019-07-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2019.06.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Modulating inflammation for cancer therapy.

    Ritter, Birgit / Greten, Florian R

    The Journal of experimental medicine

    2019  Volume 216, Issue 6, Page(s) 1234–1243

    Abstract: A link between chronic inflammation and development of tumors is well established. Moreover, it has become evident that tumorigenesis is not a cell autonomous disease, and an inflammatory microenvironment is a prerequisite of basically all tumors, ... ...

    Abstract A link between chronic inflammation and development of tumors is well established. Moreover, it has become evident that tumorigenesis is not a cell autonomous disease, and an inflammatory microenvironment is a prerequisite of basically all tumors, including those that emerge in the absence of overt inflammation. This knowledge has led to the development of anti-inflammatory concepts to treat and prevent cancer. In contrast, immunotherapies, in particular checkpoint inhibitors, representing the most significant progress in the therapy of several malignancies depend on the presence of a pro-inflammatory "hot" environment. Here, we discuss pro- and anti-inflammatory concepts for the treatment of cancer.
    MeSH term(s) Animals ; Humans ; Immunotherapy ; Inflammation/pathology ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Tumor Microenvironment
    Language English
    Publishing date 2019-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20181739
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: YAP1 takes over when oncogenic K-Ras slumbers.

    Greten, Florian R

    Cell

    2014  Volume 158, Issue 1, Page(s) 11–12

    Abstract: It is of great therapeutic importance to understand why tumors relapse after the failure of therapies targeting oncogenes to which cancer cells are addicted. In this issue, Kapoor et al. and Shao et al. identify the transcriptional coactivator YAP1 as a ... ...

    Abstract It is of great therapeutic importance to understand why tumors relapse after the failure of therapies targeting oncogenes to which cancer cells are addicted. In this issue, Kapoor et al. and Shao et al. identify the transcriptional coactivator YAP1 as a central driver of compensation for the loss of K-Ras signaling in K-Ras-dependent cancers.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Adenocarcinoma/metabolism ; Animals ; Carcinoma, Pancreatic Ductal/metabolism ; Cell Cycle Proteins ; Cell Survival ; Colonic Neoplasms/drug therapy ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition ; Humans ; Lung Neoplasms/drug therapy ; Pancreatic Neoplasms/metabolism ; Phosphoproteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins p21(ras)/metabolism ; Transcription Factors ; ras Proteins/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; KRAS protein, human ; Phosphoproteins ; Proto-Oncogene Proteins ; Transcription Factors ; YAP1 protein, human ; Yap1 protein, mouse ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2014-06-30
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2014.06.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Fungi Enter the Stage of Colon Carcinogenesis.

    Conche, Claire / Greten, Florian R

    Immunity

    2018  Volume 49, Issue 3, Page(s) 384–386

    Abstract: The significant contribution of intestinal bacteria for the pathogenesis of colorectal cancer is widely accepted by now. In this issue of Immunity, two articles by Malik et al. (2018) and Wang et al. (2018) highlight the role of commensal fungi, which so ...

    Abstract The significant contribution of intestinal bacteria for the pathogenesis of colorectal cancer is widely accepted by now. In this issue of Immunity, two articles by Malik et al. (2018) and Wang et al. (2018) highlight the role of commensal fungi, which so far have been underestimated.
    Language English
    Publishing date 2018-09-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2018.09.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Image-guided radiotherapy in an orthotopic mouse model of rectal cancer.

    Nicolas, Adele M / Pesic, Marina / Rödel, Franz / Fokas, Emmanouil / Greten, Florian R

    STAR protocols

    2022  Volume 3, Issue 4, Page(s) 101749

    Abstract: Radiobiology research in rectal cancer has been limited to cell lines, patient-derived organoids (PDOs), or xenografts. Here, we describe a protocol which recapitulates more efficiently the complex contributions of the tumor microenvironment. This ... ...

    Abstract Radiobiology research in rectal cancer has been limited to cell lines, patient-derived organoids (PDOs), or xenografts. Here, we describe a protocol which recapitulates more efficiently the complex contributions of the tumor microenvironment. This approach establishes a preclinical mouse model of rectal cancer by intrarectal transplantation of genetically modified organoids into immunocompetent mice followed by precise image-guided radiotherapy (IGRT) of organoid-induced tumors. This model represents a useful platform to study the cellular and molecular determinants of therapy resistance in rectal cancer. For complete details on the use and execution of this protocol, please refer to Nicolas et al. (2022).
    MeSH term(s) Humans ; Mice ; Animals ; Radiotherapy, Image-Guided/methods ; Rectal Neoplasms ; Disease Models, Animal ; Heterografts ; Tumor Microenvironment
    Language English
    Publishing date 2022-10-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2022.101749
    Database MEDical Literature Analysis and Retrieval System OnLINE

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