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  1. Book ; Online: Self-Eating on Demand: Autophagy in Cancer and Cancer Therapy

    Lane, Jon D. / Agostinis, Patrizia

    2018  

    Abstract: Macroautophagy, the major lysosomal pathway for recycling intracellular components including whole organelles, has emerged as a key process modulating tumorigenesis, tumor-stroma interactions, and cancer therapy. An impressive number of studies over the ... ...

    Abstract Macroautophagy, the major lysosomal pathway for recycling intracellular components including whole organelles, has emerged as a key process modulating tumorigenesis, tumor-stroma interactions, and cancer therapy. An impressive number of studies over the past decade have unraveled the plastic role of autophagy during tumor development and dissemination. The discoveries that autophagy may either support or repress neoplastic growth and contextually favor or weaken resistance and impact antitumor immunity have spurred efforts from many laboratories trying to conceptualize the complex role of autophagy in cancer using cellular and preclinical models. This complexity is further accentuated by recent findings highlighting that various autophagy-related genes have roles beyond this catabolic mechanism and interface with oncogenic pathways, other trafficking and degradation mechanisms and the cell death machinery. From a therapeutic perspective, knowledge of how autophagy modulates the tumor microenvironment is crucial to devise autophagy-targeting strategies using smart combination of drugs or anticancer modalities. This eBook contains a collection of reviews by autophagy researchers and provides a background to the state-of-the-art in the field of autophagy in cancer, focusing on various aspects of autophagy regulation ranging from its molecular components to its cell autonomous role, e.g. in cell division and oncogenesis, miRNAs regulation, cross-talk with cell death pathways as well as cell non-autonomous role, e.g. in secretion, interface with tumor stroma and clinical prospects of autophagy-based biomarkers and autophagy modulators in anticancer therapy. This eBook is part of the TransAutophagy initiative to better understand the clinical implications of autophagy in cancer
    Keywords Medicine (General) ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens
    Size 1 electronic resource (111 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020099616
    ISBN 9782889454228 ; 2889454223
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Endoplasmic reticulum stress in health and disease

    Agostinis, Patrizia / Samali, Afshin

    2012  

    Author's details Patrizia Agostinis ; Samali Afshin (ed.)
    Language English
    Size VIII, 452 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT017381353
    ISBN 978-94-007-4350-2 ; 9789400743519 ; 94-007-4350-5 ; 9400743513
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: Decoding immunogenic cell death from a dendritic cell perspective

    Janssens, Sophie / Rennen, Sofie / Agostinis, Patrizia

    Immunological Reviews. 2024 Jan., v. 321, no. 1 p.350-370

    2024  

    Abstract: Dendritic cells (DCs) are myeloid cells bridging the innate and adaptive immune system. By cross‐presenting tumor‐associated antigens (TAAs) liberated upon spontaneous or therapy‐induced tumor cell death to T cells, DCs occupy a pivotal position in the ... ...

    Abstract Dendritic cells (DCs) are myeloid cells bridging the innate and adaptive immune system. By cross‐presenting tumor‐associated antigens (TAAs) liberated upon spontaneous or therapy‐induced tumor cell death to T cells, DCs occupy a pivotal position in the cancer immunity cycle. Over the last decades, the mechanisms linking cancer cell death to DC maturation, have been the focus of intense research. Growing evidence supports the concept that the mere transfer of TAAs during the process of cell death is insufficient to drive immunogenic DC maturation unless this process is coupled with the release of immunomodulatory signals by dying cancer cells. Malignant cells succumbing to a regulated cell death variant called immunogenic cell death (ICD), foster a proficient interface with DCs, enabling their immunogenic maturation and engagement of adaptive immunity against cancer. This property relies on the ability of ICD to exhibit pathogen‐mimicry hallmarks and orchestrate the emission of a spectrum of constitutively present or de novo‐induced danger signals, collectively known as damage‐associated molecular patterns (DAMPs). In this review, we discuss how DCs perceive and decode danger signals emanating from malignant cells undergoing ICD and provide an outlook of the major signaling and functional consequences of this interaction for DCs and antitumor immunity.
    Keywords adaptive immunity ; cell death ; dendritic cells ; neoplasm cells
    Language English
    Dates of publication 2024-01
    Size p. 350-370.
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note REVIEW
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.13301
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: Decoding immunogenic cell death from a dendritic cell perspective.

    Janssens, Sophie / Rennen, Sofie / Agostinis, Patrizia

    Immunological reviews

    2023  Volume 321, Issue 1, Page(s) 350–370

    Abstract: Dendritic cells (DCs) are myeloid cells bridging the innate and adaptive immune system. By cross-presenting tumor-associated antigens (TAAs) liberated upon spontaneous or therapy-induced tumor cell death to T cells, DCs occupy a pivotal position in the ... ...

    Abstract Dendritic cells (DCs) are myeloid cells bridging the innate and adaptive immune system. By cross-presenting tumor-associated antigens (TAAs) liberated upon spontaneous or therapy-induced tumor cell death to T cells, DCs occupy a pivotal position in the cancer immunity cycle. Over the last decades, the mechanisms linking cancer cell death to DC maturation, have been the focus of intense research. Growing evidence supports the concept that the mere transfer of TAAs during the process of cell death is insufficient to drive immunogenic DC maturation unless this process is coupled with the release of immunomodulatory signals by dying cancer cells. Malignant cells succumbing to a regulated cell death variant called immunogenic cell death (ICD), foster a proficient interface with DCs, enabling their immunogenic maturation and engagement of adaptive immunity against cancer. This property relies on the ability of ICD to exhibit pathogen-mimicry hallmarks and orchestrate the emission of a spectrum of constitutively present or de novo-induced danger signals, collectively known as damage-associated molecular patterns (DAMPs). In this review, we discuss how DCs perceive and decode danger signals emanating from malignant cells undergoing ICD and provide an outlook of the major signaling and functional consequences of this interaction for DCs and antitumor immunity.
    MeSH term(s) Humans ; Immunogenic Cell Death ; Dendritic Cells ; Cell Death ; Neoplasms ; Antigens, Neoplasm ; Adaptive Immunity
    Chemical Substances Antigens, Neoplasm
    Language English
    Publishing date 2023-12-13
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.13301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: BNIP3 in melanoma: isn't it IRONic?

    Vara-Pérez, Mónica / Agostinis, Patrizia

    Molecular & cellular oncology

    2021  Volume 8, Issue 4, Page(s) 1947169

    Abstract: Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α) ...

    Abstract Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α) levels and melanoma growth
    Language English
    Publishing date 2021-08-02
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2021.1947169
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: ER-mitochondria contact sites; a multifaceted factory for Ca

    Sassano, Maria Livia / Felipe-Abrio, Blanca / Agostinis, Patrizia

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 988014

    Abstract: Membrane contact sites (MCS) between organelles of eukaryotic cells provide structural integrity and promote organelle homeostasis by facilitating intracellular signaling, exchange of ions, metabolites and lipids and membrane dynamics. Cataloguing MCS ... ...

    Abstract Membrane contact sites (MCS) between organelles of eukaryotic cells provide structural integrity and promote organelle homeostasis by facilitating intracellular signaling, exchange of ions, metabolites and lipids and membrane dynamics. Cataloguing MCS revolutionized our understanding of the structural organization of a eukaryotic cell, but the functional role of MSCs and their role in complex diseases, such as cancer, are only gradually emerging. In particular, the endoplasmic reticulum (ER)-mitochondria contacts (EMCS) are key effectors of non-vesicular lipid trafficking, thereby regulating the lipid composition of cellular membranes and organelles, their physiological functions and lipid-mediated signaling pathways both in physiological and diseased conditions. In this short review, we discuss key aspects of the functional complexity of EMCS in mammalian cells, with particular emphasis on their role as central hubs for lipid transport between these organelles and how perturbations of these pathways may favor key traits of cancer cells.
    Language English
    Publishing date 2022-08-16
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.988014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Methods for Isolation of Tumor-Associated Endothelial Cells for Surface Protein Analysis and Sorting by Flowcytometry.

    Verhoeven, Jelle / Agostinis, Patrizia / Agrawal, Madhur

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2572, Page(s) 45–54

    Abstract: Polychromatic flowcytometry is increasingly used for simultaneously analyzing multiple intracellular and cell-surface proteins on a given cell population. Here we describe a flowcytometry-based method to analyze various proteins on the surface of ... ...

    Abstract Polychromatic flowcytometry is increasingly used for simultaneously analyzing multiple intracellular and cell-surface proteins on a given cell population. Here we describe a flowcytometry-based method to analyze various proteins on the surface of endothelial cells (which comprise of less than 0.5% of the tumor microenvironment) and concurrently sort the live endothelial cells for the downstream applications such as gene expression by conventional quantitative PCR or by single-cell RNA sequencing.
    MeSH term(s) Cell Count ; Endothelial Cells/pathology ; Flow Cytometry/methods ; Humans ; Membrane Proteins ; Neoplasms/pathology ; Tumor Microenvironment
    Chemical Substances Membrane Proteins
    Language English
    Publishing date 2022-09-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2703-7_3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Eating your own fat to stay fit: lipophagy sustains lymphangiogenesis.

    Mece, Odeta / Houbaert, Diede / Agostinis, Patrizia

    Autophagy

    2022  Volume 19, Issue 4, Page(s) 1351–1353

    Abstract: Lymphatic endothelial cells (LECs) exploit fatty acid oxidation (FAO) to grow and to maintain lymphatic vessel identity through the epigenetic regulation of the essential transcription factor PROX1. In our recent study, we found that LEC-specific loss ... ...

    Abstract Lymphatic endothelial cells (LECs) exploit fatty acid oxidation (FAO) to grow and to maintain lymphatic vessel identity through the epigenetic regulation of the essential transcription factor PROX1. In our recent study, we found that LEC-specific loss of
    MeSH term(s) Mice ; Animals ; Lymphangiogenesis ; Endothelial Cells/metabolism ; Epigenesis, Genetic ; Acetyl Coenzyme A/metabolism ; Homeodomain Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Autophagy ; Inflammation/metabolism ; Mice, Knockout ; Fatty Acids/metabolism
    Chemical Substances Acetyl Coenzyme A (72-89-9) ; Homeodomain Proteins ; Tumor Suppressor Proteins ; Fatty Acids
    Language English
    Publishing date 2022-09-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2117513
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Diversifying the platinum-based chemotherapy toolkit for immunogenic cancer cell death.

    Garg, Abhishek D / Agostinis, Patrizia

    Oncotarget

    2020  Volume 11, Issue 36, Page(s) 3352–3353

    Language English
    Publishing date 2020-09-08
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.27713
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The "Yin and Yang" of Unfolded Protein Response in Cancer and Immunogenic Cell Death.

    Rufo, Nicole / Yang, Yihan / De Vleeschouwer, Steven / Agostinis, Patrizia

    Cells

    2022  Volume 11, Issue 18

    Abstract: Physiological and pathological burdens that perturb endoplasmic reticulum homeostasis activate the unfolded protein response (UPR), a conserved cytosol-to-nucleus signaling pathway that aims to reinstate the vital biosynthetic and secretory capacity of ... ...

    Abstract Physiological and pathological burdens that perturb endoplasmic reticulum homeostasis activate the unfolded protein response (UPR), a conserved cytosol-to-nucleus signaling pathway that aims to reinstate the vital biosynthetic and secretory capacity of the ER. Disrupted ER homeostasis, causing maladaptive UPR signaling, is an emerging trait of cancer cells. Maladaptive UPR sustains oncogene-driven reprogramming of proteostasis and metabolism and fosters proinflammatory pathways promoting tissue repair and protumorigenic immune responses. However, when cancer cells are exposed to conditions causing irreparable ER homeostasis, such as those elicited by anticancer therapies, the UPR switches from a survival to a cell death program. This lethal ER stress response can elicit immunogenic cell death (ICD), a form of cell death with proinflammatory traits favoring antitumor immune responses. How UPR-driven pathways transit from a protective to a killing modality with favorable immunogenic and proinflammatory output remains unresolved. Here, we discuss key aspects of the functional dichotomy of UPR in cancer cells and how this signal can be harnessed for therapeutic benefit in the context of ICD, especially from the aspect of inflammation aroused by the UPR.
    MeSH term(s) Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Humans ; Immunogenic Cell Death ; Neoplasms/metabolism ; Unfolded Protein Response
    Language English
    Publishing date 2022-09-16
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11182899
    Database MEDical Literature Analysis and Retrieval System OnLINE

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