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  1. Article ; Online: An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks.

    Alfaro-García, Jenny Paola / Granados-Alzate, María Camila / Vicente-Manzanares, Miguel / Gallego-Gómez, Juan Carlos

    Cells

    2021  Volume 10, Issue 11

    Abstract: Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and ... ...

    Abstract Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and other types of viruses drive genetic and epigenetic changes that expand the tumorigenic program, including modifications to the ability of cancer cells to migrate. The best-characterized group of changes is collectively known as the epithelial-mesenchymal transition, or EMT. This is a complex phenomenon classically described using biochemistry, cell biology and genetics. However, these methods require enormous, often slow, efforts to identify and validate novel therapeutic targets. Systems biology can complement and accelerate discoveries in this field. One example of such an approach is Boolean networks, which make complex biological problems tractable by modeling data ("nodes") connected by logical operators. Here, we focus on virus-induced cellular plasticity and cell reprogramming in mammals, and how Boolean networks could provide novel insights into the ability of some viruses to trigger uncontrolled cell proliferation and EMT, two key hallmarks of cancer.
    MeSH term(s) Animals ; Cell Plasticity/genetics ; Cellular Reprogramming/genetics ; Epithelial-Mesenchymal Transition/genetics ; Gene Regulatory Networks ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Systems Biology ; Virus Diseases/genetics ; Virus Diseases/pathology ; Viruses/classification ; Viruses/pathogenicity
    Language English
    Publishing date 2021-10-24
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10112863
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: An Integrated View of Virus-Triggered Cellular Plasticity Using Boolean Networks

    Jenny Paola Alfaro-García / María Camila Granados-Alzate / Miguel Vicente-Manzanares / Juan Carlos Gallego-Gómez

    Cells, Vol 10, Iss 2863, p

    2021  Volume 2863

    Abstract: Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and ... ...

    Abstract Virus-related mortality and morbidity are due to cell/tissue damage caused by replicative pressure and resource exhaustion, e.g., HBV or HIV; exaggerated immune responses, e.g., SARS-CoV-2; and cancer, e.g., EBV or HPV. In this context, oncogenic and other types of viruses drive genetic and epigenetic changes that expand the tumorigenic program, including modifications to the ability of cancer cells to migrate. The best-characterized group of changes is collectively known as the epithelial–mesenchymal transition, or EMT. This is a complex phenomenon classically described using biochemistry, cell biology and genetics. However, these methods require enormous, often slow, efforts to identify and validate novel therapeutic targets. Systems biology can complement and accelerate discoveries in this field. One example of such an approach is Boolean networks, which make complex biological problems tractable by modeling data (“nodes”) connected by logical operators. Here, we focus on virus-induced cellular plasticity and cell reprogramming in mammals, and how Boolean networks could provide novel insights into the ability of some viruses to trigger uncontrolled cell proliferation and EMT, two key hallmarks of cancer.
    Keywords cellular plasticity ; epithelial–mesenchymal transition ; systems biology ; Boolean ; viral infection ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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