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. 2008 Jan 8;98(2):245–249. doi: 10.1038/sj.bjc.6604087

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Copyright © 2008 Cancer Research UK

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The prostate microenvironment and influence of senescence on carcinogenesis. (A) The normal microenvironment involves reciprocal paracrine interactions between epithelium and constituents of the stroma (fibroblasts, smooth muscle, endothelium, matrix, and inflammatory cells (not shown)) that serve to maintain homoeostasis and a functional differentiated tissue state. Microenvironmental signalling maintains tissue homoeostasis. (B) Cellular damage in the context of chronological ageing and/or oxidative stress leads to the accumulation of senescent stromal cells, which produce paracrine-acting factors capable of inducing or promoting epithelial carcinogenesis. (C) Continued promotion of carcinogenesis by the altered microenvironment, including changes in the matrix components, contributes to invasive and metastatic epithelial cell phenotypes. Aberrant paracrine signals from initiated epithelial cells also contribute to further stromal senescence and/or the development of a reactive stroma that further influences carcinogenesis.