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• W2074328794 abstract "Ras/Raf-prototypic oncogenes induce cellular senescence, a terminal cell-cycle arrest, as a default cellular safeguard program, while oncogenic Myc is known to rather promote apoptosis as the prime failsafe mechanism. We review and discuss here evidence for Myc-induced senescence - which is detectable to a limited degree as a cell-autonomous, direct response to Myc action, but occurs predominantly in a non-cell-autonomous fashion via crosstalk of the oncogene-driven cell population with non-neoplastic bystanders, namely cells of the host immune system, prompting them to release pro-senescent cytokines that strike back onto adjacent proliferating tumor cells. In particular, we discuss how Myc-evoked apoptosis serves as a signal for macrophage attraction and activation, followed by the secretion of TGF-β as a cytokine that is capable of terminally arresting Myc-driven lymphoma cells without causing further DNA damage and without launching a senescence-associated, pro-inflammatory, and, therefore, potentially detrimental cytokine response in the target population. In essence, non-cell-autonomous but still oncogene-orchestrated senescence is a functionally relevant, robustly tumor-suppressive principle with critical implications for conceptually novel anti-cancer therapies in the clinic." @default.
• W2074328794 created "2016-06-24" @default.
• W2074328794 creator A5008229579 @default.
• W2074328794 creator A5013921170 @default.
• W2074328794 creator A5040330310 @default.
• W2074328794 date "2011-12-01" @default.
• W2074328794 modified "2023-10-14" @default.
• W2074328794 title "The Myc/macrophage tango: Oncogene-induced senescence, Myc style" @default.
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• W2074328794 doi "https://doi.org/10.1016/j.semcancer.2011.10.002" @default.
• W2074328794 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22019769" @default.
• W2074328794 hasPublicationYear "2011" @default.
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