© 1991 Oxford University Press
Glutathione S-transferase mu locus: use of genotyping and phenotyping assays to assess association with lung cancer susceptibility
Shan Zhong,
A. Forbes Howie 1,
Brian Ketterer 2,
John Taylor 2,
John D. Hayes 1,
Geoffrey J. Beckett 1,
Christopher G. Wathen 4,
C.Roland Wolf 4 and
Nigel K. Spurr 5
Human Genetic Resources, Imperial Cancer Research Fund, Clare Hall Laboratories Blanche Lane, South Mimms, Potters Bar, Herts EN6 3LD
1Department of Clinical Chemistry, University of Edinburgh Edinburgh Royal Infirmary. Edinburgh EH3 9YW
2CRC Molecular Toxicology Group, Department of Biochemistry, University College and Middlesex School of Medicine Windeyer Building, Cleveland Street, London WIP 6DB
3Department of Medicine, University of Edinburgh Edinburgh Royal Infirmary, Edinburgh EH3 9YW
4ICRF Molecular Pharmacology Group, Hugh Robson Buildmg, University of Edinburgh George Square, Edinburgh EH8 9XD, UK
5To whom correspondence should be addressed
In mammals, the cytosolic glutathione S-transferases (GSTs; EC 2.5.1.18) are a supergene family comprised of four multigene families, named alpha, mu, pi and theta. In man, withn the mu class gene family there is a gene (the GSTmu 1 locus) that is polymorphic and is only expressed in 50–55% of individuals. It has previously been reported, using transstilbene oxide (tSBO) as a specific substrate for the expressed phenotype, that smokers with the null phenotype had a greater susceptibility to lung cancer. In a subsequent study, it was shown that on Southern blot analyses of human DNAs using a GSTmu 1 cDNA probe a DNA fragment was absent in certain individuals. The absence of this band correlated with the tSBO null phenotype. In the present work, DNA clones derived from GST mu class genomic sequences were used as probe in Southern blot analyses and confirmed the correlation between the lack of a DNA fragment and the null phenotype; moreover in this case, using radioimmunoassay for the GST mu protein, these probes were then used in a genotyping assay to investigate further the association of GSTmu 1 polymorphism with susceptibility to lung cancer. It was found that in a control group of 225 individuals, of unknown smoking history, 42% lacked the restriction fragment and were homozgous null, and therefore 58% were either heterozygous or were homozygous normal. Among 228 lung cancer patients, which included all tumour types, a similar distribution occurred, namely 43% were homozygous and 57% were heterozygous or homozygous normal. If, however, the tumours were analysed by tumour type a small but significant positive correlation with the homozygous null genotype was seen in squamous carcinoma of the lung, and an apparently negative correlation with adenocarcinoma of the lung.
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