IBTISSEM MOUNA BOUDOKHANE, MOHAMED EL-HADEF EL-OKKI, AMARIA AOUAR, SOUMIA MEDJANI, OUARDA SEMMAME, TAHA FILALI, ASMA MIMOUNI, KARIMA SIFI, NOUREDDINE ABADI AND DALILA SATTA
Abstract
It is widely known that lung carcinoma is an environment-related sickness that develops as a consequence of exposure to mutagenic sellers, especially those present in tobacco. The CYP1A1 gene codifies the phase I enzyme aryl hydrocarbon hydroxylase (AHH) belonging to the cytochrome P450 machine that plays a pivotal role in the bio-activation of tobacco procarcinogens. Greater enzymatic activity is associated with the CYP1A1 mL polymorphism (T6235C transition) and has been described as a genetic susceptibility factor for lung cancer. This case-control study was carried out to verify if this association holds in a study population of 80 lung cancer patients and 85 controls from Eastern Algeria. Genetic polymorphisms were determined by Restriction Fragment Length Polymorphism (RFLP) assay. The frequencies of the genotypes CYP1A1 m1 in both groups were investigated to get odds ratios and 95 % confidence intervals. The TC Genotype and C allele were significantly higher in patients compared to healthy controls with [OR = 0.547 (0.235- 1.241), p = 0.130], and [OR = 0.536 (0.245 - 1.135), p = 0.083] respectively. However, these two factors were not found to be significantly associated with the risk of lung cancer. After stratification of the population according to tobacco consumption, non-smokers were at higher risk compared with smokers [OR = 0.086 (0.007 - 0.550), p = 0.003]. Our findings support the conclusion that CYP1A1m1 polymorphism does not seem to be associated with susceptibility to lung cancer in Eastern Algeria.