Prospects for skin cancer treatment and prevention: the potential contribution of an engineered virus

J Invest Dermatol. 2011 Mar;131(3):559-61. doi: 10.1038/jid.2010.394.

Abstract

Nonmelanoma skin cancers are among the most common human malignancies. Although typically not lethal, they are responsible for tissue deformity and substantial morbidity, particularly in high-risk populations. Solar UVB radiation-a major etiologic factor for this kind of malignancy-produces DNA lesions such as cyclobutane pyrimidine dimers and 6-4 photoproducts in skin. These lesions are removed through nucleotide excision repair because humans lack a DNA glycosylase required to initiate base excision repair of pyrimidine-pyrimidine photoproducts but produce all the other proteins required for this process. In this issue, Johnson et al. show that a DNA glycosylase derived from Chlorella virus and engineered to enhance tissue penetration and nuclear localization can remove UVB-induced DNA lesions in a human skin equivalent model and that the protein can be incorporated into a topical formulation for the prevention and treatment of UVB-induced DNA damage. These results suggest that such an enzyme may be incorporated into regimens for the chemoprevention of skin cancers.

Publication types

  • Comment
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Administration, Topical
  • Biomedical Engineering*
  • Carcinoma, Basal Cell / drug therapy
  • Carcinoma, Basal Cell / prevention & control
  • Carcinoma, Squamous Cell / drug therapy
  • Carcinoma, Squamous Cell / prevention & control
  • Chlorella*
  • DNA Damage / drug effects
  • DNA Glycosylases / administration & dosage
  • DNA Glycosylases / pharmacology
  • DNA Repair / drug effects
  • Humans
  • Skin Neoplasms / drug therapy*
  • Skin Neoplasms / prevention & control*
  • Ultraviolet Rays / adverse effects

Substances

  • DNA Glycosylases