Publication year: 2011 Source: Seminars in Cancer Biology, Available online 13 October 2011 Soyoung Lee, Clemens A. Schmitt, Maurice Reimann 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 fashionviacrosstalk 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.
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The Myc/macrophage tango: oncogene-induced senescence, Myc style.