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​Classical carcinogenesis theory has an initiation event, followed by a series of promotional events. The model for this has been clearly demonstrated in animals for the ultraviolet light induction of squamous carcinoma. An initiation event such as a sunburn is far more likely to produce a squamous carcinoma if there are a series of subsequent promotional events, such as further sunburns. Presumably the initial DNA damage can only carry a cell a certain way towards a full expression of a cancer, but multiple other abnormalities must be induced before the final expression of that cancer.

The viral induction of squamous carcinoma, such as that caused by oncogenic papilloma virus infections, may or may not follow such a pathway in, for instance the development of squamous carcinoma of the cervix.

Squamous carcinoma occurring in chronic wounds is presumably on the basis of an induced high mitotic rate, coupled with chronic inflammatory reaction. The exact cellular mechanisms are unknown.

The etiology of basal cell carcinoma and melanomas not nearly so well worked out. There is no good animal model for basal carcinoma. While melanoma has been noted in experimental systems using the fish and the nose of the opossum, the relevance of these findings to man is questionable.

We do know that both basal cell carcinoma and melanoma are most significantly linked to early exposure to ultraviolet light. Squamous carcinoma on the other hand is linked to total lifetime exposure, with the past ten years exposure being very important, and total exposure levels being even more important. Both melanoma and basal cell carcinoma have a rapidly accelerating relative risk with relatively low exposures, followed by a broad plateau.

Indeed, outdoor workers with a very large exposure to ultraviolet light have a slightly lower risk of melanoma than indoor workers episodically significantly exposed to ultraviolet light. In other words the carcinogenesis patterns for basal cell carcinoma and melanoma on one hand, and squamous cell carcinoma on the other are fundamentally different.

Ultraviolet B (UVB), with wavelengths between 280 and 320 nanometers, is felt to be the most significant cause of all three types of skin cancer. UVB, the burning and carcinogenic wavelengths of light, is blocked by window glass. Wavelengths below 280 nanometers (ultraviolet C) are blocked by the ozone layer.

UVB exerts its damage directly on DNA, and that effect is directly related to dosage intensity. UVB can cause such damage at lower levels than that causing clinical sunburns.

Between UVB and visible light is ultraviolet A. Ultraviolet A is 320 to 400 nanometers, the beginning of visible light. Ultraviolet A has two types of energies within it. Between 320 and 340 nanometers is UVA of sufficient similarity to UVB to cause direct DNA damage. UVB and UVA up to 340 nanometers are carcinogenic. Between 340 and 400 nanometers there is pure UVA type damage, which is indirect through an effect of other molecules on DNA. The UVA activates photoactive molecules in the cell that in turn damage the DNA. Pure UVA effect is much less carcinogenic than UVB. Pure UVA can cause tanning and is an important cause of photoaging, and is the specific cause of what has been termed UVA wrinkling and sagging of the skin (see photoaging). In other words, ultraviolet A as a broad band is not just a tanning wavelength, it includes some UVB like activity at one end of its spectrum, and a more pure UVA like activity at the other. The major UVA effect is to cause tanning and UVA photoaging effects such as UVA sagging of the skin.

SOURCE: Carcinogenesis ( )
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