Premium
DNA repair capacity as a risk factor for non‐melanocytic skin cancer—a molecular epidemiological study
Author(s) -
Hall Janet,
English Dallas R.,
Artuso Marina,
Armstrong Bruce K.,
Winter Michael
Publication year - 1994
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910580206
Subject(s) - transfection , dna repair , basal cell carcinoma , microbiology and biotechnology , biology , skin cancer , chloramphenicol acetyltransferase , reporter gene , dna damage , population , confidence interval , cell , plasmid , dna , gene , cancer , immunology , gene expression , medicine , pathology , genetics , basal cell , environmental health
Capacity to repair UV‐induced DNA damage was studied by use of a host cell reactivation assay in T lymphocytes isolated from 86 cases and 87 controls (aged 44‐68 years) who were participants in a population‐based case‐control study of basal cell (BCC) or squamous cell (SCC) carcinoma of the skin in Geraldton, Western Australia. Lymphocytes were cultured and transfected with either control or UV‐irradiated plasmids (254 mm, 350 J/m 2 ) containing a reporter gene [the chloramphenicol‐acetyltransferase ( CAT ) gene], and the repair capacity was determined by measuring CAT gene expression in protein extracts prepared from the transfected cells. DNA repair activity was 1.07 (95% confidence interval 0.94‐1.26) times greater in BCC cases than in controls for each 350 J/m 2 increment in UV dose to the plasmids, and 1.04 (95% confidence interval 0.85‐1.26) times greater in SCC cases than in controls, though the differences were not statistically significant. DNA repair activity showed little association with age, sex and viability of the lymphocytes, though it was positively associated with their blastogenic rate ( p =0.055).