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dc.contributor.authorVella, V.
dc.contributor.authorDe Francesco, E. M.
dc.contributor.authorBonavita, Eduardo
dc.contributor.authorLappano, R.
dc.contributor.authorBelfiore, A.
dc.date.accessioned2022-08-01T09:07:03Z
dc.date.available2022-08-01T09:07:03Z
dc.date.issued2022en
dc.identifier.citationVella 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.en
dc.identifier.pmid35691786en
dc.identifier.doi10.1016/j.tem.2022.04.009en
dc.identifier.urihttp://hdl.handle.net/10541/625371
dc.description.abstractType 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.en
dc.language.isoenen
dc.relation.urlhttps://dx.doi.org/10.1016/j.tem.2022.04.009en
dc.titleIFN-I signaling in cancer: the connection with dysregulated Insulin/IGF axisen
dc.typeArticleen
dc.contributor.departmentEndocrinology Unit, Department of Clinical and Experimental Medicine, University of Catania, Garibaldi-Nesima Hospital, 95122 Catania, Italyen
dc.identifier.journalTrends in Endocrinology and Metabolismen
dc.description.noteen]


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