The dark side of sunlight and melanoma

See allHide authors and affiliations

Science  20 Feb 2015:
Vol. 347, Issue 6224, pp. 824
DOI: 10.1126/science.aaa6578

You are currently viewing the summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution


Skin cancer is the most prevalent form of cancer, with a lifetime risk of 1 in 5 for Americans (1). Most skin cancers can be attributed to C→T and CC→TT mutations in DNA resulting from cyclobutane pyrimidine dimers (CPDs) produced by the direct absorption of UVB light (290 to 320 nm) present in sunlight (2). The most generally accepted mechanism for the formation of these mutations is that Cs or 5-methyl-Cs in the CPDs rapidly deaminate to Us or Ts, which are then replicated in an error-free manner. One might expect that photodamage would cease once out of the Sun, but Premi et al., on page 842 of this issue, show that this is not the case in melanocytes (3). A substantial fraction of UV damage to DNA in these cells may be occurring in the dark, by a novel pathway with important implications for melanoma formation.