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Molecular Basis of Skin Carcinogenesis

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The Molecular Basis of Human Cancer

Abstract

p53 tumor suppressor gene is the most commonly mutated gene in human and mouse cancers. Disruption of the p53 and Rb pathways is a fundamental property of most human cancer cells. Inactivation of CDKN2A can lead to deregulation of these two pathways. Genetic abnormalities in CDKN2A gene have been well documented in human melanoma but their involvement in human non-melanoma skin cancer (NMSC) is less clear. Several studies have shown that NMSC harbor unique mutations in the p53 gene as well as inactivation of the CDKN2A gene. While mutations in the p53 gene are induced by UV radiation and represent tumor-initiating events, the majority of alterations detected in the CDKN2A gene do not appear to be UV-dependent. In conclusion, in addition to p53 mutations, silencing of other tumor suppressor genes such as the CDKN2A gene might play a significant role in NMSC development.

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Correspondence to Alessia Pacifico M.D. .

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Pacifico, A., Leone, G., Ananthaswamy, H.N. (2017). Molecular Basis of Skin Carcinogenesis. In: Coleman, W., Tsongalis, G. (eds) The Molecular Basis of Human Cancer. Humana Press, New York, NY. https://doi.org/10.1007/978-1-59745-458-2_29

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