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The inflammatory network: bridging senescent stroma and epithelial tumorigenesis Shan W; Yang G; Liu JFront Biosci (Landmark Ed) 2009[Jan]; 14 (11): 4044-57Cellular senescence or aging, defined by permanent cell cycle arrest, is well known for its evolutionary advantage in protecting the organism from developing cancer; however, it is also acknowledged that aged stromal cells can significantly expedite epithelial tumorigenesis, although exactly how they function to augment tumor formation remains elusive. Recent evidence suggests that this tumor-promoting effect is likely mediated by diffusible pro-inflammatory molecules synthesized and released by senescent stromal fibroblasts, acting in a paracrine fashion on adjacent tumor epithelium. Mobilization of the inflammatory network by senescent fibroblasts has bifurcated roles on the epithelial and stromal compartments, converging on the promotion of epithelial tumorigenesis. A thorough understanding of the regulatory mechanisms underlying these events may lead to improved approaches in cancer treatment.|*Cell Transformation, Neoplastic[MESH]|Cellular Senescence[MESH]|Epithelial Cells/*pathology[MESH]|Humans[MESH]|Inflammation/*pathology[MESH]|Neoplasms, Glandular and Epithelial/*pathology[MESH]|Stromal Cells/*pathology[MESH] |
