SUSCEPTIBILITY TO ORAL SQUAMOUS CELL CARCINOMA:
CORRELATION WITH VARIANTS OF CYP1A1-MspI, GSTT1,
GSTM1, ALDH2, EC-SOD AND LIFESTYLE FACTORS
Dong T-T, Wang L-J, Liu L-Z, Ma S-N
*Corresponding Author: Mrs. Ting-Ting Dong, General Hospital of Daqing Oil Field, No. 9 Zhongkang Street, Saertu District,
Daqing 163001, Heilongjiang Province, Peoples Republic of China. Tel: +86-459-599-4114. Fax: +86-459-580-5247.
Email: tingtingdong_139@163.com
page: 61
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RESULTS
Oral Squamous Cell Carcinoma and Lifestyle.
General demographic and clinical information for participants
in both groups are provided in Table 1. There was no
statistically significant difference in gender or age between
case and control groups (p >0.05). However, smoking and
drinking were significantly more common in individuals
with OSCC than in controls (p <0.01).
Genotype Distribution. For each of the enzyme
encoding genes we investigated, the distribution of genotypes,
significantly differed between cases and controls (all
p <0.01). CYP1A1-MspI (m2/m2), EC-SOD (C/G), GSTT1
[], GSTM1 [] and ALDH2 (non G/G) genotypes were
significantly more common in individuals with OSCC than
in control individuals (p <0.01) (Table 2).
Multiple Genotype Variants Distribution. Because
there was a significant shift of the genotype frequencies observed
in individuals with OSCC compared to controls, we
also examined whether OSCC patients were more likely to
carry multiple variant genotypes than healthy subjects. The
combined distribution of CYP1A1-MspI (m2/ m2), ECSOD (C/G), GSTT1 [], GSTM1 [] and ALHD2 (non G/G)
genotypes in both groups are provided in Table 3. Within
the patient group, the majority of individuals (90.4%) had
at least two of the variants. Namely, 1.9% of individuals
were positive for five of the variant genotypes, 20.8% for
four genotypes, 37.1% for three genotypes, 30.7% for
two genotypes, 8.5% for only one variant genotype, and
only 1.1% did not have any of the variant genotypes. In
contrast, in the control group, the majority of individuals
had one or no variants (51.6%). Thus, the presence of two
or more variants in the OSCC population was significantly
more common than in controls (p <0.01).
Smoking Status and Gene Polymorphisms. Table
4 depicts the results of the analysis of CYP1A1-MspI (m2/
m2), EC-SOD (C/G), GSTT1 [], GSTM1 [] and ALHD2
(non G/G) variant genotype presence and smoking status.
In individuals with OSCC, multiple variants and smoking
were significantly more common compared to the control
group; smoking in combination with multiple variant
genotypes had a synergistic effect on cancer likelihood.
Smokers with five variant genotypes were 32-times more
likely to have OSCC.
Furthermore, within the sub-population of smokers,
SI was synergistic with multiple variant genotypes (Table
5). In the patient group, the presence of multiple variant
genotypes and an SI >400 was significantly more common
compared to the control group (p <0.01).
Drinking Status and Gene Polymorphisms. A
similar analysis was applied to CYP1A1-MspI (m2/m2),
EC-SOD (C/G), GSTT1 [], GSTM1 [] and ALHD2 (non
G/G) variant genotypes and alcohol consumption (Table 6).
The presence of multiple variants and alcohol consumption
was significantly more common in patients compared
to the control group; furthermore, as with smoking, the
drinking behavior and combined variant genotypes had a
synergistic effect on the likelihood of cancer.
The synergistic effect of the DI and combined expression
of variant genotypes is depicted in Table 7. In the
patient group, the presence of multiple variants and a DI
>3000 was significantly more common compared to the
control group (p <0.01).
Analysis of Combined Smoking/Drinking Status
and Gene Polymorphisms. Table 8 displays the results of
the analysis of the presence of variant genotypes combined
with smoking and drinking status. In the patient group,
there were significantly more patients who had multiple
variants and were positive for both smoking and drinking
history as compared to the control group.
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