The aim of this study was to evaluate whether beta-catenin accumulation is useful for diagnosing the malignant potential of oral precancerous lesions. We investigated oral epithelial dysplasia adjacent to early cancer induced by 4-nitroquinoline 1-oxide in rats. Localization of beta-catenin and cell proliferation were detected immunohistochemically, and exon 3 of the beta-catenin gene was analyzed. Accumulation of beta-catenin in the cytoplasm and nucleus was evident in 10 of 16 dysplasia lesions. Since almost all of the dysplastic lesions in these rats transformed to invasive cancer, beta-catenin accumulation may contribute to the early stage of carcinogenesis. The Ki-67 labeling index was significantly higher in dysplasia and early cancer than in no change. However, there were no significant differences between the expression patterns of beta-catenin protein, suggesting that other proliferation pathways are involved in the early stage of tumor development in addition to beta-catenin accumulation. No mutations of exon 3 of the beta-catenin gene were detected in any of the dysplasia or early cancer lesions. These findings suggested that beta-catenin accumulation in the cytoplasm and nucleus without mutation of exon 3 is an early event during carcinogenesis in this tongue cancer model.