ArticleGeroScience2026
Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.
Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
Senescence is a tripartite cellular phenotype characterized by permanent growth arrest, resistance to apoptosis, and high secretory activity. Besides its physiological role in embryonic development and pathophysiological contribution to age-related tissue degeneration, in the context of tumor development senescence is an important suppressor mechanism, that counteracts accelerated proliferation. Among the many stressors that induce senescence is the external stimulation by cytokines. Although cytokine-induced senescence (CIS) has repeatedly been reported in the literature, the signaling networks leading to the senescent phenotype remained enigmatic. Here, we used two models of tumor-associated (TA)-CIS: (i) in vitro treatment of human A204 cancer cells with interferon (IFN)-γ and tumor necrosis factor (TNF) and (ii) in vivo senescence induction by adoptive transfer of T helper 1 (T
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