Molecular epidemiology of skin cancers: DNA repair and non-melanocytic skin cancer.
Exposure to sunlight has been clearly associated with non-melanocytic skin cancer, however individual susceptibility differs considerably. Ethnic origin and pigmentary characteristics are generally accepted as risk factors. Another important defense mechanism is the ability to repair DNA photoproducts. In the inherited disorder xeroderma pigmentosum the inability to repair such DNA damage, associated with a high incidence of skin cancers, suggests an important role for DNA repair capacity in the etiology of this cancer. The development of an in vitro repair assay based on human peripheral blood lymphocytes, has allowed the evaluation of DNA repair capacity as a risk factor in population based studies. This article reviews recent developments in this field.
Hall
J
J
International Agency for Research on Cancer, Lyon, France.
Artuso
M
M
English
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DR
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000528:radiation effects; D003043:Cocarcinogenesis; D003057:Cockayne Syndrome / Q000235:genetics; D004249:DNA Damage; D004260:DNA Repair / Q000235:genetics; D006801:Humans; D015994:Incidence; D008322:Mammals / Q000235:genetics; D009381:Neoplasms, Radiation-Induced / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics; D010787:Photosensitivity Disorders / Q000235:genetics; D011740:Pyrimidine Dimers / Q000378:metabolism; D012307:Risk Factors; D012878:Skin Neoplasms / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics; D013472:Sunlight / Q000009:adverse effects*; D014466:Ultraviolet Rays / Q000009:adverse effects; D014983:Xeroderma Pigmentosum / Q000235:genetics
D011740:Pyrimidine Dimers