• Login
    View Item 
    •   Home
    • The Christie Research Publications Repository
    • All Christie Publications
    • View Item
    •   Home
    • The Christie Research Publications Repository
    • All Christie Publications
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of ChristieCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsThis CollectionTitleAuthorsIssue DateSubmit DateSubjects

    My Account

    LoginRegister

    Local Links

    The Christie WebsiteChristie Library and Knowledge Service

    Statistics

    Display statistics

    IFN-I signaling in cancer: the connection with dysregulated Insulin/IGF axis

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Authors
    Vella, V.
    De Francesco, E. M.
    Bonavita, Eduardo
    Lappano, R.
    Belfiore, A.
    Affiliation
    Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Catania, Garibaldi-Nesima Hospital, 95122 Catania, Italy
    Issue Date
    2022
    
    Metadata
    Show full item record
    Abstract
    Type I interferons (IFN-Is) are prototypical inflammatory cytokines produced in response to stress. IFN-Is have a critical role in antitumor immunity by driving the activation of leukocytes and favoring the elimination of malignant cells. However, IFN-I signaling in cancer, specifically in the tumor microenvironment (TME), can have opposing roles. Sustained IFN-I stimulation can promote immune exhaustion or enable tumor cell-intrinsic malignant features. Herein, we discuss the potential impact of the insulin/insulin-like growth factor system (I/IGFs) and of metabolic disorders in aberrant IFN-I signaling in cancer. We consider the possibility that targeting I/IGFs, especially in patients with cancer affected by metabolic disorders, contributes to an effective strategy to inhibit deleterious IFN-I signaling, thereby restoring sensitivity to various cancer therapies, including immunotherapy.
    Citation
    Vella V, De Francesco EM, Bonavita E, Lappano R, Belfiore A. IFN-I signaling in cancer: the connection with dysregulated Insulin/IGF axis. Vol. 33, Trends in Endocrinology & Metabolism. Elsevier BV; 2022. p. 569–86.
    Journal
    Trends in Endocrinology and Metabolism
    URI
    http://hdl.handle.net/10541/625371
    DOI
    10.1016/j.tem.2022.04.009
    PubMed ID
    35691786
    Additional Links
    https://dx.doi.org/10.1016/j.tem.2022.04.009
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.tem.2022.04.009
    Scopus Count
    Collections
    All Christie Publications

    entitlement

    Related articles

    • Paracrine recruitment and activation of fibroblasts by c-Myc expressing breast epithelial cells through the IGFs/IGF-1R axis.
    • Authors: De Vincenzo A, Belli S, Franco P, Telesca M, Iaccarino I, Botti G, Carriero MV, Ranson M, Stoppelli MP
    • Issue date: 2019 Nov 15
    • Insulin-like growth factors inhibit dendritic cell-mediated anti-tumor immunity through regulating ERK1/2 phosphorylation and p38 dephosphorylation.
    • Authors: Huang CT, Chang MC, Chen YL, Chen TC, Chen CA, Cheng WF
    • Issue date: 2015 Apr 1
    • A candidate targeting molecule of insulin-like growth factor-I receptor for gastrointestinal cancers.
    • Authors: Adachi Y, Yamamoto H, Ohashi H, Endo T, Carbone DP, Imai K, Shinomura Y
    • Issue date: 2010 Dec 14
    • Insulin-like growth factor-1 signaling in the tumor microenvironment: Carcinogenesis, cancer drug resistance, and therapeutic potential.
    • Authors: Nwabo Kamdje AH, Seke Etet PF, Kipanyula MJ, Vecchio L, Tagne Simo R, Njamnshi AK, Lukong KE, Mimche PN
    • Issue date: 2022
    • Insulin-like growth factor receptor signaling in tumorigenesis and drug resistance: a challenge for cancer therapy.
    • Authors: Hua H, Kong Q, Yin J, Zhang J, Jiang Y
    • Issue date: 2020 Jun 3
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Quick Guide | Contact Us
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.