Abstract
Carcinogenesis is a multi-step process involving the accumulation of alterations within the cellular genome (reviewed in 1,2). These alterations can occur in protooncogenes converting them into activated oncogenes, and it has been suggested that the multi-step nature of carcinogenesis may partly reflect the consecutive activation of several dominantly acting oncogenes (3-7). It seems reasonable to presume that prostatic cancer follows this pattern. In support of this notion, oncogene activities have been reported to be present in human prostatic adenocarcinoma (8-10), in cell lines derived from cancerous prostatic tissues (11), and in Dunning R3327 rat prostatic adenocarcinomas (12,13). Recently, utilizing the mouse prostate reconstitution model system, it was demonstrated that activated ras or myc oncogenes singly were able to induce distinct dysplastic and hyperplastic lesions, respectively (14). The two oncogenes in combination induced rapidly growing, poorly differentiated malignant adenocarcinomas. Thus, the activation of the ras and myc oncogenes can induce a step-like progression of carcinogenesis in this experimental animal model.
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Thompson, T.C. et al. (1991). Evidence for the Involvement of Genetic Differences and Mesenchymal Factors in the Progression of Oncogene-Induced Prostate Cancer in Reconstituted Mouse Prostate. In: Karr, J.P., Coffey, D.S., Smith, R.G., Tindall, D.J. (eds) Molecular and Cellular Biology of Prostate Cancer. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3704-5_37
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DOI: https://doi.org/10.1007/978-1-4615-3704-5_37
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