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Human ocular surface squamous neoplasia (OSSN) is the most common ocular surface precancerous and cancerous lesion previously known by various names such as conjunctival intraepithelial neoplasia, corneal intraepithelial neoplasia (CIN), or both together (CCIN) (Grossniklaus et al., 1987). Clinically, OSSN manifests in different grades ranging from simple dysplasia to squamous cell carcinoma (Grossniklaus et al., 1987). Because of the high incidence of OSSN in the limbal area, where the corneal epithelial stem cells are located, the limbal transition zone/stem cell theory has been proposed for the development of CIN by Lee and Hirst (Lee and Hirst, 1995). Tseng and co-investigators have suggested that the slow cycling limbal stem cells may become hyper-proliferative by stimulations such as alterations in this anatomic site influenced by other factors, e.g., carcinogens, irradiation (eg, UVB), and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA) (Tseng, 1989), which can cause abnormal proliferation of the conjunctival and corneal epithelium and lead to the formation of CIN. Nevertheless, the etiology and pathogenesis of CIN and ocular surface carcinoma remain elusive. To date, there is no appropriate animal model available to study the molecular and cellular mechanisms of this disease. Therefore, the availability of such animal model will not only aid to understand the pathogenesis but also yield a more effective treatment for OSSN.

Excess Fibroblast Growth Factor-7 (FGF-7) Activates b-Catenin and Leads to Ocular Surface Squamous Neoplasia in Mice