[Frontiers in Bioscience 2, d538-551, November 1, 1997]

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Holly Soehnge, Allal Ouhtit and Honnavara N. Ananthaswamy

Department of Immunology, The University of Texas M D Anderson Cancer Center, 1515 Holcombe Blvd., Box 178, Houston, TX 77030

Received 10/20/97 Accepted 10/24/97


1. Abstract

2. Introduction
3. Interaction of UV radiation with the skin
3.1. The nature of the UV spectrum
3.2. UV radiation causes DNA damage and mutations
3.3. Mutations can lead to loss of cell cycle control and carcinogenesis
3.4. DNA repair and apoptosis are defenses against carcinogenesis
4. Tumor suppressor genes and oncogenes in skin cancer
4.1. The p53 tumor suppressor gene
4.1.1. p53 and the cell cycle
4.1.2. p53 and apoptosis
4.1.3. Inactivation of p53 gene
4.1.4. p53 mutations in UV-induced skin cancers
4.1.5. p53 mutations arise early during UV skin carcinogenesis
4.2. The patched (ptc) gene is a tumor suppressor in humans
4.2.1. ptc gene activity is conserved in Drosophila and vertebrates
4.2.2. ptc mutations and nevoid basal cell carcinoma syndrome
4.2.3. UV-induced patched mutations play a role in BCC development
4.3. The role of ras oncogenes in skin cancer
5. A model for UV-induction of skin cancer
6. Perspective
7. Acknowledgments
8. References
9. Entire manuscript

Key words: Sunlight, UV Carcinogenesis, Mutation, Tumor Suppressor Genes, Oncogenes, P53, Patched, Ras, Immunosuppression

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