Aging is a major risk factor for keratinocyte skin cancer. Here we investigate the impact of Age-Related alterations in the Dermal Microenvironment (ARDM) on keratinocyte skin cancer initiation/development, using a transgenic mouse model of accelerated dermal aging. This model expresses CCN1, a secreted extracellular matrix (ECM) associated protein, driven by the fibroblast collagen1A2 promoter. CCN1 is significantly elevated in dermal fibroblasts in aged human skin and is a key driver of ARDM. By six months of age, Col1a2-CCN1 mice exhibited accelerated dermal aging including dermal thinning (reduced 39%, N=6, p<0.05), loss of collagen protein content and gene expression (reduced 51% and 63%, respectively, N=5, p<0.05), and increased degradation of collagen fibrils, measured by immunostaining and atomic force microscopy, compared to control littermates. Furthermore, Col1a2-CCN1 mice exhibited increased expression of multiple matrix metalloproteinases, hepatocyte growth factor, and cytokines and reduced expression of TGF-β type II receptor (N=5, p<0.05), as observed in aged human skin. Importantly, six-month-old Col1a2-CCN1 mice displayed dramatically increased susceptibility to skin papilloma/tumor formation in two different skin tumor models; two-stage chemical carcinogenesis (N=5) and keratinocyte-targeted inducible oncogenic HRas (N=4-5, p<0.05). In both of these models, multiple papillomas/tumors occurred only in Col1a2-CCN1 mice. No papillomas/tumors were formed in littermate controls. In stark contrast, two-month-old Col1a2-CCN1 mice, before the development of ARDM, were completely resistant to papilloma/tumor formation, similar to controls. These data demonstrate that ARDM creates a tissue milieu that actively promotes keratinocyte cancer. Col1a2-CCN1 mice provide a powerful model for investigating the mechanisms by which age-related changes in the stromal microenvironment contribute to cutaneous carcinoma development in the elderly.