© 1993 Oxford University Press
Relationship between the GSTM1 genetic polymorphism and susceptibility to bladder, breast and colon cancer
S. Zhong,
A.H. Wyllie 1,
D. Barnes 2,
C.R. Wolf 3 and
N.K. Spurr 4
Biomedical Research Centre, ICRF Molecular Pharmacology Unit, Level 5 Ninewells Hospital Dundee, DD1 9SY
1The Cancer Research Campaign Laboratories, Department of Pathology, University Edinburgh, George Square, Edinburgh EH8 9XD
2ICRF Clinical Oncology Unit, Guy's Hospital London SE1 9RT
4ICRF Clare Hall Laboratories Blanche Lane, South Mimms, Potters Bar, Herts EN6 3LD, UK
3To whom correspondence should be addressed
Mammalian cytosolic glutathione S-transferases (GSTs; EC 2.5.1.18) form a supergene family consisting of four distinct families, named alpha, mu, pi and theta. In humans one member of the mu class gene family (GSTM1) has been shown to be polymorphic and is only expressed in 5560% of individuals. Previous studies have shown a possible link with the null phenotype and susceptibility to cancer, in particular to lung cancer. In this study we genotyped individuals with breast, bladder and colorectal cancer. A total of 490 individuals with cancer were studied, and consisted of 97 bladder, 197 breast and 196 colorectal cancers. No significant differences were observed in the frequency of nulled individuals in bladder or breast cancer patients when compared with a control population of 225 individuals. However, a significant excess of nulled individuals were seen in colorectal cancer: 56.1% compared with the control group value of 41.8%. This was shown to be highly significant depending on the site of the tumours and >70% of individuals with a tumour in the proximal colon were GSTM1 nulled. This is an
2-fold increase in colon cancer risk in these individuals.

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