Gene Cell Tissue. 2020 July; 7(3):e103317.
Published online 2020 July 25.
doi: 10.5812/gct.103317.
Research Article
Detection of R282w P53 Gene Mutation on Exon 8 in Gastric Cancer
Patients in Southwest Iran
Sajad Afrouz
1
, Mohammad Amin Ghatee
2, *
, Amroallah Roozbehi
2
and Mohammad Hossein
Sangtarash
1
1
Department of Biological Sciences, University of Sistan and Baluchistan, Zahedan, Iran
2
Cellular and Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran
*
Corresponding author: Ph.D., Cellular and Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran. Email: ghateea1980@gmail.com
Received 2020 April 04; Revised 2020 June 15; Accepted 2020 June 27.
Abstract
Background: Gastric adenocarcinoma is the most common type of gastric cancer all around the world. The epithelial cells of stom-
ach tissue are influenced by environmental factors and genetic disorders. P53 is the most remarkable gene that controls the growth
of cells. Mutation in some nucleotides of the P53 gene increases the genetic instability and is assumed as an important prognostic
factor in gastric cancer. More than 90% of mutations occur in the exons 5-8 of p53.
Objectives: This study was conducted in Kohgiluyeh and Boyer Ahmad (K&B) province (Southwest Iran) to determine the rate of
R282W P53 gene mutation of exon 8 in gastric cancer.
Methods: This case-control study was conducted on 90 subjects that were divided into two groups (each including 45 patients and
45 controls). The samples were randomly collected from the tissue bank of the pathology laboratory in Yasuj city and then were
transferred to the Cellular and Molecular Research Center. DNA extraction was performed by the DNA extraction kit. Molecular
analysis on exon 8 was performed by the PCR-RFLP method and using the MspI restricting enzyme. Data were analyzed by descriptive
statistics and bivariate correlation tests.
Results: No difference was found between the two groups concerning age, gender, and education level. The prevalence of R282W
P53 gene mutation on exon 8 in the cancer group was 17.8% (8/45), while no mutation was found in the control group.
Conclusions: According to the results, the R282W P53 gene mutation on exon 8 may play an important role in the development of
gastric cancer in Yasuj district, Southwest Iran.
Keywords: P53, PCR, RFLP, Exon 8, R282W
1. Background
Gastric cancer (GC) is the second leading cause of
cancer-related mortality (1). Its incidence shows a wide ge-
ographical variation. About half of the total gastric cancer
load occurs in East Asia, particularly in China and Japan (2).
The low-risk areas include Southern Asia, and North and
East Africa (3). Although the incidence of GC is gradually
decreasing in many parts of the world, it is still the most
common malignancy in Iran (4). There are several inter-
mediate and low-risk populations in geographical areas,
while the northern and northwestern regions are high-
risk areas for gastric cancer (4). The mean incidence rate
of stomach cancer is 10.5 - 12 (5). Based on the previous
studies, the incidence of stomach cancer is rising in K&B
province, including in Yasuj district (6).
Regarding the marked variation of gastric cancer risk
in different geographical areas and striking differences in
frequency of possible environmental and ethnic risk fac-
tors, research on the gastric cancer etiology in each pop-
ulation should be considered as a priority (3).
GC is a multifactorial disease that develops due to con-
tinuous cell damage caused by life-long exposure to differ-
ent predisposing factors, including carcinogens (7-9). Epi-
genetic alteration involving tumor suppressor genes mu-
tations, DNA repair genes, and loss of heterozygosis (LOH)
A may cause cancerous cell mutation (10, 11). Recent stud-
ies have revealed that p53 mutations are biologically and
clinically distinct. Genetic alterations in the TP53 gene
are fundamental events in both early-stage and advanced
stomach tumors (12, 13). Approximately, over 50% of hu-
man cancers carry a loss of function mutations in the p53
gene (14) in which, 95% of TP53 mutations occur within
the genomic region encoding the sequence-specific DNA-
binding domain of TP53 protein (exons 4-9) (15-17). A mis-
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