Irradiation Carcinogenesis

A number of the points made about chemical carcinogenesis are also true for radiation-induced carcinogenesis. Both X-rays and ultraviolet (UV) radiation, for example, produce damage to DNA. As with chemical carcinogens, this damage induces DNA repair processes, some of which are error prone and may lead to mutations. The development of malignant transformation in cultured cells after irradiation requires cell proliferation to ''fix'' the initial damage into a heritable change and then to allow clonal proliferation and expression of the typical transformed phenotype.105 Fixation appears to be complete after the first postirradiation mitotic cycle. In the case of mouse C3H/10 T 1/2 cells, expression of radiation-induced transformation requires an additional 12 rounds of cell division. Thus, as in the case of chemical carcinogenesis, a promotion phase is required for full expression of the initiated malignant alteration. Moreover, when low doses of chemical carcinogens and X-rays are used together, these two types of agents act synergistically to produce malignant transformation.105

When cells are exposed to UV light in the 240 to 300 nm range, the bases acquire excited energy states, producing photochemical reactions between DNA bases (reviewed in Reference 106). The principal products in DNA at biologically relevant doses of UV light are cyclobutane dimers formed between two adjacent pyrimidine bases in the DNA chain. Both thymine-thymine and thymine-cytosine dimers are formed. That formation of these dimers is linked to mutagenic events (see below).

Heavy exposure to sunlight induces similar changes in human skin, and the degree of exposure to sunlight is closely related to the incidence of skin cancer (see Chapter 3). Whether continuing exposure to UV rays in sunlight is the promoting agent in skin cancer or additional promoting events are required is not clear, but it seems that UV irradiation is a complete carcinogen, just as some chemicals areā€”that is, it has both initiating and promoting activities. Patients who cannot efficiently repair UV-induced damage, such as those with xeroderma pigmento-sum, have a much higher risk of developing malignant skin tumors.

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