Increased lung cancer risk associated with genetic polymorphism of glutathione S-transferase (GST, EC 220.127.116.11) isozyme mu was examined in a Chinese population.
A significantly higher proportion in lung cancer patients showed GST mu deficiency compared with control group (71.0% vs. 51.1%, P<0.005).
Although the susceptibility to lung cancer showing gene deletion for GST mu isoform in non-smoking group is not significantly different from that in smoking group, a great number of individuals with gene deletion was found among cancer patients who are less than 50 years old.
The pathology of lung tumors related to that lack of class mu isoform which occurred most frequently in patients with small cell carcinomas.
Thus, present data further support that sensitivity to chemical toxins and pulmonary carcinogens may be affected by GST mu isoform polymorphism.
Mots-clés Pascal : Glutathione transferase, Transferases, Enzyme, Epidémiologie, Carcinome, Bronchopulmonaire, Homme, Chine, Asie, Mutation, Délétion, Isozyme, Carcinogène, Facteur risque, Tabac, Polluant, Déficit, Appareil respiratoire pathologie, Poumon pathologie, Bronche pathologie, Tumeur maligne, Génétique, Toxicité, Chinois, Prédisposition
Mots-clés Pascal anglais : Glutathione transferase, Transferases, Enzyme, Epidemiology, Carcinoma, Bronchopulmonary, Human, China, Asia, Mutation, Deletion, Isozyme, Carcinogen, Risk factor, Tobacco, Pollutant, Deficiency, Respiratory disease, Lung disease, Bronchus disease, Malignant tumor, Genetics, Toxicity, Chinese, Predisposition
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0236655
Code Inist : 002B11A. Création : 11/06/1997.