Scientists have elucidated the mechanisms underlying the repair of UV-induced damage in DNA, which frequently causes skin cancer. The protein structures additionally determined by these researchers will improve our understanding of how the body protects itself against skin cancer. These studies lay the foundations for the development of a new class of anti cancer agents.
Without capturing public attention, the number of new cases of skin cancer is continuously increasing. This type of cancer is now more common than breast, colon and lung cancer combined. No less discouraging is the fact that the number of deaths from skin cancer is also steadily rising - in contrast to the trends observed for many other cancers, where survival rates are improving thanks to effective treatments. But reliable treatments can only be developed if the molecular mechanisms underlying skin cancer are better understood. Here, scientists at the FMI have made an important breakthrough.
It is well known that skin cancer arises from damage caused by the sun’s ultraviolet (UV) radiation. This radiation produces mutations in DNA which influence cellular processes, possibly leading to cancer. Although the body has various strategies for repairing such damage, the most frequent type of UV lesion turns out to be particularly problematic. In this case, two components of DNA combine to form structures known as cyclobutane pyrimidine dimers (CPDs). These are difficult for the cell’s repair system to detect - partly because they are inconspicuous, given the size of the entire genome, but also because they remain hidden within tightly coiled DNA.