Ultraviolet (UV) radiation covalently links two thymine bases in the DNA strand, leading to a distorting lesion — i.e., the thymine-thymine (T-T) dimer. Photoproducts such as these are believed to cause skin cancer–producing mutations.
Recently, two groups of investigators used novel approaches to observe the crystal structure of the enzyme DNA polymerase η (Polη), which is able to replicate properly past T-T dimers, resulting in normal polymerization and less risk for cancer-producing mutations. These results also help to elucidate how Polη defects lead to the variant form of xeroderma pigmentosum XPV; patients with XPV are sensitive to solar radiation and develop many skin cancers.
The researchers observed that, like other DNA polymerases, …
Reviewing Author
DisclosuresConsultant / advisory board Lubax; WorldCare Clinical
EquityLubax
Grant / Research support NIH; Department of Defense; American Skin Association; Piramal
Editorial boardsBritish Journal of Dermatology; Journal of the American Academy of Dermatology; Journal of Investigative Dermatology
Leadership positions in professional societies American Academy of Dermatology (Chair, Skin Cancer and Melanoma Committee); American Board of Dermatology (Director)
DisclosuresConsultant / advisory board Lubax; WorldCare Clinical
EquityLubax
Grant / Research support NIH; Department of Defense; American Skin Association; Piramal
Editorial boardsBritish Journal of Dermatology; Journal of the American Academy of Dermatology; Journal of Investigative Dermatology
Leadership positions in professional societies American Academy of Dermatology (Chair, Skin Cancer and Melanoma Committee); American Board of Dermatology (Director)