الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Lung cancer remains the most lethal cancer worldwide. The mechanism of lung carcinogenesis is not understood. Although cigarette smoking is the major cause of lung cancer, not all smokers develop lung cancer. Tobacco smoke contains several carcinogens including polycyclic aromatic hydrocarbons (PAHs), N-nitrosamines, and heterocyclic amines. Cytochrome P450 (CYP) isozymes activate these environmental pollutants to yield highly reactive substances that bind to DNA, forming adducts involved in the initiation of carcinogenesis.
METHOD: Thirty cases of lung cancer and thirty controls participated in the study. The participants were screened for the presence of CYP1A1 polymorphism, namely CYP1A1*2A (MspI) by polymerase chain reaction (PCR) amplification followed by restriction enzyme digestion.
RESULT: The frequency of CYP1A1*2A genotypes TC and CC among cases group was higher than the control group (46.7%, 20% vs 26.7%, 3.3%) respectively and the frequency of C allele among cases was higher than the control group (43.3% vs 16.7%) respectively. Individual carrying TC , CC genotypes and C allele have respectively 3, 12 and 3 times increased risk to develop lung cancer (OR: 3.67 , 95% CI : 1.01-13.8 ) , (OR: 12.6 , 95% CI : 1.18-318.4) , (OR: 3.82 ,95% CI : 1.52- 9.8) respectively. Individuals carrying TC, CC genotypes and C allele in smokers of cases group have increased risk to develop lung cancer 7, 11 and 4 times than in non smokers of cases group (OR: 7.0, 95% CI: 1.0-77.92), (OR: 11.67, 95%CI: 1.0- 426.0), (OR: 4.31, 95%CI: 1.13-17.32) respectively.
CONCLUSION: The results suggest that CYP1A1*2A gene polymorphism have increased the risk of developing lung cancer with an interaction between CYP1A1*2A gene polymorphism and smoking. Keywords: CYP1A1, Lung cancer, PCR.
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