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Skin cancer’s DNA legacy

Many bacteria and some mammalian cells can repair damage caused to their DNA by ultraviolet and ionising radiation by removing damaged regions and replacing them. The failure of such repair mechanisms is responsible for one form of malignant skin disease.

Two types of DNA repair mechanism exist, and these are called photoreactivation and dark repair. The former is the simpler, acting only on UV damage and functioning only in light. The second is termed dark repair because cells with this ability can repair their DNA in the dark. This is a more useful mechanism to a cell than photoreactivation, but it is more complicated because it involves several enzymes.

In bacteria, the DNA molecule is being continuously monitored for structural defects and, within the genetic capability of the cell, any unsatisfactory regions are replaced by dark repair. It now seems that a dark repair mechanism of this sort also operates in mammalian cells. Recent experiments have shown human cells from most tissues can repair damaged bases in DNA by excision and replacement, following either exposure to UV light or large X-ray doses.

That this process has a survival value is shown by the human disease known as xeroderma pigmentosum. This is a genetically determined condition in which the skin fibroblasts – unlike those in normal individuals – cannot repair damage to their DNA. This leads to a fatal form of skin cancer. Thus an understanding of an apparently esoteric aspect of molecular biology is helping our understanding of human cancer.

From New ÐÓ°ÉÔ­´´, 20 March 1969