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, People’s Republic of China. Tel: +86-459-599-4114. Fax: +86-459-580-5247.
Email: tingtingdong_139@163.com
page: 61
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DISCUSSION
The pathogenesis of OSCC is complex, involving
combined action of a variety of environmental and genetic
factors [11-13]. Smoking and drinking are the main
risk factors for OSCC [14,15]. Our findings confirm that
smoking and drinking were significantly more frequent
in individuals with OSCC than in the control individuals.
Heavy cigarette and alcohol consumption were also
significantly higher in the OSCC group compared to the
control group.
The CYP1A1 is a member of the cytochrome P450
family involved in the metabolism of exogenous materials,
encoding aryl hydrocarbon hydrolase (AHH), and activating
polycyclic aromatic hydrocarbon and aromatic amine
[16]. Our results showed that the distribution of genotypes
for CYP1A1-MspI was significantly different between the
patient group and the control group, and that the CYP1A1-
MspI (m2/m2) genotype may increase susceptibility to
OSCC. This finding, aligned with prior studies, shed light
on the involvement of the CYP1A1-MspI polymorphism in
carcinogenesis through modified enzymatic activity [16].
Our results also confirmed the results of a meta-analysis
which found that CYP1A1-MspI increased the odds of
OSCC, specifically among Asian populations [30].
Superoxide dismutase is generally considered as the
first line antioxidative defense in the body [17]. This enzyme
can be highly effective against ROS to protect the
cells and tissues from oxidative stress [18]. The SOD dysregulation
is correlated with growth of human malignant
tumors [19,20]. Further, EC-SOD appears to be important
for tumor formation [21-23], and is correlated with OSCC
[24]. Our study mirrored the earlier studies that indicated
EC-SOD association with OSCC and showed a significant
difference in distribution of EC-SOD genotypes between
the patient and control groups [24].
The GST polymorphisms are also correlated with cancer
susceptibility. Glutathione S-transferase can catalyze
the binding of electrophilic carcinogens and glutathione,
to metabolize compounds that are easily soluble in water
and excrete them. GSTM1/GSTT1 has been previously
associated with susceptibility to oral carcinomas [25,31].
Our study confirmed that GSTM1[–]/GSTT1[–] genotypes
are correlated with susceptibility to OSCC.
Animal studies have found that the in vivo metabolite
of ethanol, acetaldehyde, has significant carcinogenic effects
[26,27], and ALDH2 is the main enzyme to metabolize
acetaldehyde in the liver. Furthermore, ALDH2 gene polymorphism
is correlated with a variety of tumors [28-30,32].
Our study confirmed the correlation between ALDH2 (non
G/G) genotypes and increased susceptibility to OSCC.
Interestingly, our study also found significant differences
in the prevalence of combined CYP1A1-MspI
(m2/ m2), EC-SOD (C/G), GSTT1 [–], GSTM1 [–] and
ALHD2 (non G/G) variant genotypes between the patient
and control groups. In the patient group, the percentage
of patients with a combination of variant genotypes (more
than two genotypes) was significantly higher than that of
the control group; the relative risks of OSCC in such patients
were significantly increased. Previous studies have
shown that OSCC patients are more likely to carry multiple
variants and have a history of smoking or drinking; the
interaction of two or more of these factors enhances risk
[3,5,29, 30,32]. Our simultaneous analyses confirmed these
previous results, as individuals with both multiple variant
genotypes and a smoking and drinking history exhibited
a significantly higher risk of OSCC. Therefore, OSCC
risk increases with the increasing amount and period of
smoking and drinking.
Further investigations and studies of the effects of these
gene and environmental interactions is paramount to an
earlier diagnosis of OSCC. More studies of non Asian populations
is another avenue of research worth undertaking.
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