Abstract
Cytochrome P450 2E1 (CYP2E1) is a key enzyme involved in the metabolic activation of procarcinogens such as N-nitrosoamines and low-molecular-weight organic compounds. The main aim of this study was to determine whether CYP450 2E1 polymorphisms are associated with the risk of colorectal cancer (CRC). We investigated the genotype distribution of the CYP2E1 gene RsaI and a 96-base pair (bp) insertion in 86 CRC cases in comparison with 160 healthy subjects. We found the frequency of the CYP2E1 RsaI genotype to be 53.5 per cent (46/86) for c1/c1, 17.4 per cent (15/86) for c1/c2 and 29.1 per cent (25/86) for c2/c2, and the CYP2E1 98-bp insertion frequencies to be 63.9 per cent (55/86) for non-insertion (i/i), 22.1 per cent (19/86) for heterozygous insertion (i/I) and 36.0 per cent (12/86) for homozygous insertion (I/I) among CRC cases. We also found the CYP2E1 RsaI c2/c2 and CYP2E1 98-bp heterozygous i/I genotypes to be significantly associated with an increased risk of CRC (p = 0.01). We suggest that CYP2E1 polymorphisms are involved in the susceptibility to developing CRC in the ethnic Kashmiri population.
Highlights
Colorectal cancer (CRC) is one of the major causes of mortality and morbidity, and is the fourth most common cancer in men and the third most common cancer in women worldwide.[1]
Among the CRC cases, we found the frequency of the Cytochrome P450 2E1 (CYP2E1) RsaI genotype to be 53.5 per cent (46/86) for c1/c1, 17.4 per cent (15/86) for c1/c2 and 29.1 per cent (25/86) for c2/c2, while the frequency in the general control population was 70.0 per cent (112/160) for c1/c1, 12.5 per cent (20/ 160) for c1/c2 and 17.5 per cent (28/160) for c2/c2
We found the frequency of the CYP2E1 RsaI genotype to be 53.5 per cent (46/86) for c1/c1, 17.4 per cent (15/86) for c1/c2 and 29.1 per cent (25/86) for c2/c2 among CRC cases, and the CYP2E1 RsaI polymorphism to be significantly associated with the risk of CRC ( p, 0.05)
Summary
Colorectal cancer (CRC) is one of the major causes of mortality and morbidity, and is the fourth most common cancer in men and the third most common cancer in women worldwide.[1]. Epidemiological studies on various populations have shown that an increased risk of developing GIT cancers is associated with diet.[2,7,8] One important hypothesis that has received a large amount of attention is that N-nitroso compounds from dietary sources are involved in the carcinogenesis of GIT cancer.[9,10] It is known that most exogenous (xenobiotics) and endogenous chemical carcinogens require biotransformation to activated forms to be carcinogenic.[11,12] Most of the enzymes involved in drug metabolism are genetically polymorphic, and these polymorphisms may affect enzyme activity or inducibility.[13,14,15]
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