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Considering the recognized importance of PAI\u20101 in the regulation of tumor angiogenesis and invasion in murine models of skin tumor transplantation, we explored the functional significance of PAI\u20101 during early stages of neoplastic progression in the transgenic mouse model of multistage epithelial carcinogenesis (K14\u2010HPV16 mice). We have studied the effect of genetic deletion of PAI\u20101 on inflammation, angiogenesis, lymphangiogenesis and tumor progression. In this model, PAI\u20101 deficiency neither impaired keratinocyte hyperproliferation or tumor development nor affected the infiltration of inflammatory cells and development of angiogenic or lymphangiogenic vasculature. We are reporting evidence for concomitant lymphangiogenic and angiogenic switches independent to PAI\u20101 status. Taken together, these data indicate that PAI\u20101 is not rate limiting for neoplastic progression and vascularization during premalignant progression, or that there is a functional redundancy between PAI\u20101 and other tumor regulators, masking the effect of PAI\u20101 deficiency in this long\u2010term model of multistage epithelial carcinogenesis.<\/jats:p>","DOI":"10.1002\/ijc.25326","type":"journal-article","created":{"date-parts":[[2010,3,15]],"date-time":"2010-03-15T15:24:24Z","timestamp":1268666664000},"page":"283-293","source":"Crossref","is-referenced-by-count":16,"title":["Unimpeded skin carcinogenesis in K14\u2010HPV16 transgenic mice deficient for plasminogen activator 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