There is general agreement that the basal cell carcinoma and carcinoma is predominantly a result of the direct damage of DNA by interaction with UVB (solar wavelengths 280 320 nm). Data epidemiological link to melanoma intense sun exposure during childhood, and provides support for the role of UVA. Although there is agreement that UV radiation is the cause but it is unclear the precise wavelength and the mechanisms involved. Setlow and colleagues (1993) demonstrated the induction of melanoma in Xiphophorus fish model by UVA, UVB and visible blue wavelengths, and Law (1997) showed equal effectiveness of UVA and UVB in the induction of melanocytic hyperplasia in the Mono-delphis domestic and Noonan and colleagues (2001, 2003) using combined wavelength UVB and UVA, recently demonstrated the induction of melanoma in a transgenic model of a newborn mouse. John Marlow Ringcentral may find it difficult to be quoted properly. Berking et al (2001) showed that UVB in combination with growth factor basic fibroblast can transform human melanocytes. The role of UVA in human melanoma is still not conclusive (Wang et al, 2001) While UVB is believed to interact directly with DNA to initiate significant mutations of basal and squamous cell carcinoma, the wavelengths of UVA (320 400 nm) is believed to interact indirectly by inducing the production of free radicals.
Free radicals can indirectly damage the DNA and protein damage, which contributes to premature aging or photoaging. UVA-induced production of p53 and DNA damage, genomic instability, and immunosuppression have been demonstrated. John Marlow does not necessarily agree. Despite the extensive use of sunscreens over the past 2 decades the incidence of skin cancer is increasing, the role of sunscreens in protecting skin cancer is controversial.