and HBeAg(-) patients - World Journal of Gastroenterology

Table 2 Distribution of N-acetyltransferase 2 polymorphism and the risk of cancer
Genetic polymorphism NAT2 a
analysis reported a strong association between smoking
and the development of CRC [12] . However, smoking is
currently not recognized as a risk factor for CRC by the
International Agency for Research on Cancer (IARC) or
the US Surgeon General [12] . Sørensen et al [21] studied the
association between NAT1 and NAT2 polymorphisms,
smoking, meat consumption and CRC risk in 379 cancer
patients and 769 healthy subjects. In that study, only the
NAT1 polymorphism affected cancer risk. However, the
NAT1 and NAT2 fast acetylation phenotype increased the
risk of CRC among patients who smoked more cigarettes,
suggesting that N-acetylation status affects the relationship
between smoking and CRC risk.
In the present study, most subjects in the two groups
had never smoked, but the rate of ex-smokers was higher
in the case group than in the control group. Once diagnosed
with cancer, individuals tend to break old habits
that may affect the prognosis and treatment of the disease
even if it is not possible to reverse the previous damage.
The slow acetylation phenotype was more frequent among
smokers of the case group, suggesting an increased risk
of cancer (OR: 1.97, 95% CI: 1.02-3.79) in subjects with
this phenotype. A higher frequency of the slow acetylation
phenotype among patients with lung and bladder cancer
has been demonstrated in other studies. Carcinogens
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Cancer, n (%) Control, n (%) P OR (95% CI)
All 147 212
Mx/Mx 88 (59.8) 110 (51.9) 0.19 1
W/Mx 44 (30.0) 83 (39.1) 0.66 (0.42-1.05)
W/W 15 (10.2) 19 (8.9) 0.99 (0.47-2.05)
Slow 88 (59.8) 110 (51.9) 0.17 1.38 (0-2.12)
Fast 59 (40.1) 102 (48.1)
Female 76 127
Mx/Mx 42 (55.2) 58 (45.6) 0.07 1
W/Mx 23 (30.2) 58 (45.6) 0.55 (0.29-1.02)
W/W 11 (14.4) 11 (8.6) 1.38 (0.55-3.48)
Slow 42 (55.2) 58 (45.6) 0.24 1.47 (0.83-2.60)
Fast 34 (44.7) 69 (54.3)
Male 71 85
Mx/Mx 46 (64.8) 52 (61.1) 0.67 1
W/Mx 21 (29.5) 25 (29.4) 0.95 (0.47-1.92)
W/W 4 (5.6) 8 (9.4) 0.57 (0.16-2.00)
Slow 46 (64.7) 52 (61.1) 0.76 0.86 (0.45-1.65)
Fast 25 (35.2) 33 (38.9)
a Homozygous individuals with genotype W/W, and heterozygote W/Mx, are grouped into fast acetylation phenotype, while homozygous Mx/Mx are
grouped in slow acetylators. The percentages of data are in parentheses. NAT2: N-acetyltransferase 2; OR: Odds ratio; 95% CI: Confidence interval.
Table 3 Comparison between meat intake and risk of of cancer
in rapid acetylator patients n (%)
Cancer Control P OR Lower 95% CI /
upper
All 59 102
High meat intake 1 44 (74.5) 60 (58.8) 0.06 2.05 1.01/4.16
Low meat intake 2 15 (25.5) 42 (41.2)
1 More than 3 time per week; 2 Less than 3 times a week. OR: Odds ratio;
95% CI: Confidence interval.
Silva TD et al . NAT2 and colorectal cancer
Table 4 Correlation between genotypes and risk for cancer
in smokers or ex-smokers
Genetic
polymorphism
Cancer,
n (%)
Control,
n (%)
P OR (95% CI)
NAT2 a
All 65 87
Mx/Mx 40 (61.5) 39 (44.8) 0.09 1
W/Mx 22 (33.8) 39 (44.8) 1.82 (0.92-3.60)
W/W 3 (4.6) 9 (10.3) 3.08 (0.77-12.22)
Slow 40 (61.5) 39 (44.8) 0.06 1.97 (1.02-3.79)
Fast 25 (38.5) 48 (61.0)
a Homozygous individuals with genotype W/W, and heterozygote W/Mx,
are grouped into fast acetylation phenotype, while homozygous Mx/Mx
are grouped in slow acetylators. NAT2: N-acetyltransferase 2; OR: Odds
ratio; 95% CI: Confidence interval.
present in tobacco are metabolized by NAT enzymes and
activation of these enzymes is reduced in slow acetylators,
thus increasing the risk of cancer [22] .
An association between red meat consumption and
a higher risk of CRC has been reported in case-control
studies, prospective epidemiological studies and in a recent
meta-analysis [23] . The last study suggested that this
increased risk is due to the production of polycyclic aromatic
hydrocarbons and heterocyclic amines when meat is
cooked at high temperatures [24] .
Tamer et al [25] , studying 125 patients with CRC and 82
healthy subjects, observed an association between NAT2
polymorphisms and cancer development. In that study,
high protein intake was found to be correlated with an increased
risk of colon cancer (OR: 1.73, 95% CI: 1.10-3.07).
Patients with the NAT2 * 14A (M4 allele) fast acetylation
phenotype and high meat intake presented an increased
risk of CRC (OR: 3.03, 95% CI: 1.56-5.86). In the present
study, the risk of cancer was higher among patients consuming
meat more than 3 times per week (OR: 1.65, 95%
763 February 14, 2011|Volume 17|Issue 6|