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Here, we represent inflamm\u2010aging as a breakdown in the multi\u2010shell cytokine network, in which stem cells and stromal fibroblasts (referred to as the stem cell niche) become pro\u2010inflammatory cytokine over\u2010expressing cells due to the accumulation of DNA damage. Inflamm\u2010aging self\u2010propagates owing to the capability of pro\u2010inflammatory cytokines to ignite the DNA\u2010damage response in other cells surrounding DNA\u2010damaged cells. Macrophages, the major cellular player in inflamm\u2010aging, amplify the phenomenon, by broadcasting pro\u2010inflammatory signals at both local and systemic levels. On the basis of this, we propose that inflamm\u2010aging is a major contributor to the increase in cancer incidence and progression in aged people. Breast cancer will be presented as a paradigmatic example for this relationship.<\/jats:p>","DOI":"10.1002\/bies.201100104","type":"journal-article","created":{"date-parts":[[2011,11,17]],"date-time":"2011-11-17T05:58:48Z","timestamp":1321509528000},"page":"40-49","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":79,"title":["Inflamm\u2010aging of the stem cell niche: Breast cancer as a paradigmatic 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