Clinical epidemiology of gastric cancer

Ang, Tiing Leong; Fock, Kwong Ming

doi:10.11622/smedj.2014174

Cited by 312 publications

(253 citation statements)

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“…Gastric cancer is a multifactorial disorder, in which genetic and environmental interactions serve an important role in development and progression (2). Increasing age, gender, lifestyle, dietary regime, environmental factors and Helicobacter pylori infections are among the known risk factors for stomach cancer (3,4). While dietary regime and lifestyle are the most recognized factors, more effective identification of the genetic risk factors is expected to improve understanding of the basic molecular events involved in tumorigenesis (5).…”

Section: Introductionmentioning

confidence: 99%

Association of P53 gene polymorphism with gastric cancer in Northern Iran as a high‑risk region

et al. 2018

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Abstract. Gastric cancer has the fourth highest morbidity rate of all cancers worldwide. Genetic factors including alterations in oncogenes and tumor suppressor genes serve an important role in gastric cancer development and progression. The P53 gene acts as a tumor suppressor gene by regulating the cell cycle, DNA transcription and repair, apoptosis, senescence and genome stability. In addition to somatic P53 mutations in cancer development, germline polymorphisms are also involved in different malignancies. The polymorphism of P53 at codon 72 (Arg72Pro) is established as a common variant that increases susceptibility to various cancers. The present case-control study was conducted to evaluate the possible association between this P53 polymorphism and gastric cancer in the Iranian population. A total of 59 patients with gastric cancer and 59 healthy controls were enrolled in the present study. Genomic DNA was extracted from peripheral blood mononuclear cells and genotype analysis was performed using a polymerase chain reaction-based restriction fragment length polymorphism assay. Genotype frequencies did not differ significantly between the patients and controls (P=0.4); the frequencies of the three genotypes Arg/Arg, Arg/Pro and Pro/Pro in gastric cancer patients were 28.8, 49.2 and 22.0%, and in controls were 37.3, 49.2 and 13.6%. Additionally, there were no differences in genotype frequencies based on tumor location, histological differentiation or tumor stage. Based on these findings, it may be concluded that the P53 codon 72 polymorphism does not contribute to gastric cancer susceptibility in Northern Iran. IntroductionGastric cancer has the third highest mortality and fourth highest morbidity rates of all cancers worldwide (1). In 2012, GloboCan statistics reported almost 1 million new cases of gastric cancer, and more than 700,000 mortalities caused by gastric cancer (1). Gastric cancer is a multifactorial disorder, in which genetic and environmental interactions serve an important role in development and progression (2). Increasing age, gender, lifestyle, dietary regime, environmental factors and Helicobacter pylori infections are among the known risk factors for stomach cancer (3,4). While dietary regime and lifestyle are the most recognized factors, more effective identification of the genetic risk factors is expected to improve understanding of the basic molecular events involved in tumorigenesis (5). Various genetic and epigenetic changes that have the potential to convert normal epithelial cells in the stomach into malignant neoplasms may be responsible for the development of both familial and sporadic gastric cancer (6,7). Studies performed recently have demonstrated that a high number of genes and various environmental factors are the causal agents of gastric cancer, and the presence of different forms of alleles in genes (polymorphisms) may promote the development of cancers; in this regard, the P53 gene has been a research focus due to its role as a major tumor suppressor gene (8,9). The P53 ge...

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Section: Introductionmentioning

confidence: 99%

Association of P53 gene polymorphism with gastric cancer in Northern Iran as a high‑risk region

et al. 2018

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“…Genomically stable tumours were diagnosed at an earlier age, whereas MSI tumours were diagnosed at relatively older ages [7]. MSI patients tended to be female, but most EBV-positive GCs were observed in males [2]. Approximately 10% of GCs appear to have a familial predisposition, of which about half can be attributed to hereditary germline mutations as follows: hereditary diffuse gastric cancer with E-cadherin (CDH1) mutation, gastric adenocarcinoma and proximal polyposis of the stomach (implicated genes are unknown), hereditary nonpolyposis colorectal cancer (HNPCC) with mismatch repair (MMR) gene mutations, Li-Fraumeni syndrome with TP53 mutation, Peutz-Jeghers syndrome with STK11 gene mutation and Familial adenomatous polyposis with APC gene mutation [4,9,[12][13][14].…”

Section: Molecular Classification Of Gastric Cancermentioning

confidence: 99%

“…More than 70% of cases (677,000) occur in developing countries, (456,000 in men and 221,000 women), with half of the world's total coming from Eastern Asia; mainly China [1]. The age standardised incidence rate for males is generally twice that for females [2] and the majority of GCs arise in the distal stomach (non-cardia gastric cancers) with their incidence gradually decreasing throughout the world [2]. Cancers of the gastric cardia are most commonly reported in European and North American populations with a rising prevalence [2].…”

Section: Introductionmentioning

confidence: 99%

“…The age standardised incidence rate for males is generally twice that for females [2] and the majority of GCs arise in the distal stomach (non-cardia gastric cancers) with their incidence gradually decreasing throughout the world [2]. Cancers of the gastric cardia are most commonly reported in European and North American populations with a rising prevalence [2]. GC is clinically classified as early or advanced stage to help determine prognosis and appropriate treatment.…”

Section: Introductionmentioning

confidence: 99%

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Genetic and histological subtypes of gastric cancer reviewed, particularly emphasising on microsatellite instability and E-cadherin gene mutation

Karpińska-Kaczmarczyk

Lewandowska²,

Urasińska³

2017

Nowotwory. Journal of Oncology

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Almost one million new cases of gastric cancer (GC) were estimated globally in 2012, (i.e. 952,000, representing 6.8% of the total cancer burden), making it the fifth most common malignancy in the world. GC represents a biologically and genetically diverse group of tumours with multifactorial aetiologies; both environmental and genetic. The vast majority of GCs are adenocarcinomas, which can be further subdivided into intestinal and diffuse histological subtypes according to the Lauren classification published in 1965. The molecular classification of GC according to the Cancer Genome Atlas (TCGA) divides GC into four subtypes: tumours positive for the EBV virus (9%), microsatellite unstable tumours (22%), genomically stable tumours (20%) and tumours with chromosomal instability (CIN) at 50%. Most GCs are sporadic by nature, where approximately 10% appear to possess a familial predisposition of which around half can be attributed to hereditary germline mutations i.e. those of the E-cadherin (CDH1) or mismatch repair (MMR) genes. Histopathological characteristics of the tumour type and analysis of potential genetic changes have substantial clinical significance, as they determine the choice of treatment. In this review, we consider the molecular pathogenesis, phenotype and testing of GC placing particular emphasis on microsatellite instability (MSI) and the CDH1 mutation.

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“…More than 70% of cases (677,000 cases) occur in developing countries (456,000 in men, 221,000 in women), and half of the world total occurs in Eastern Asia (mainly in China) (IARC, 2012). The development of gastric cancer is correlated with various risk factors, including genetic predisposition, environmental factors, and microbial infections (Ang and Fock, 2014;Daniyal et al, 2015;Fang et al, 2015). Helicobacter pylori infection, for example, is an important risk factor for the development of gastric cancer (Graham and Yamaoka, 2000;Ang and Fock, 2014;Fang et al, 2015), but several single nucleotide polymorphisms (SNPs) are also associated with gastric carcinogenesis (Kamangar et al, 2006;Yuzhalin, 2011).…”

Section: Introductionmentioning

confidence: 99%

Association between ERCC5 gene polymorphisms and gastric cancer risk in a Chinese population

Liu

et al. 2016

Genet. Mol. Res.

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ABSTRACT. We conducted a hospital-based case-control study to investigate the association between 3 common SNPs in the ERCC5 gene (rs1047768, rs751402, and rs17655) and the risk of developing gastric cancer. Between January 2013 and December 2014, samples were collected from 216 gastric cancer patients and 216 control subjects. ERCC5 rs1047768, rs751402, and rs17655 polymorphisms were genotyped by polymerase chain reaction combined with restriction fragment length polymorphism analysis. By conditional logistic regression analysis, the GG genotype of rs17655 was found to be associated with an elevated risk of gastric cancer in a codominant model, and the adjusted OR (95%CI) was 1.96 (1.10-3.50). Moreover, in a dominant model, the CG + GG genotype of rs17655 was correlated with an increased risk of gastric cancer compared to the CC genotype (OR = 1.48; 95%CI = 1.00-2.22). rs1047768 and rs751402 were not significantly correlated with an increased or decreased gastric cancer risk.

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Clinical epidemiology of gastric cancer

Cited by 312 publications

References 70 publications

Association of P53 gene polymorphism with gastric cancer in Northern Iran as a high‑risk region

Association of P53 gene polymorphism with gastric cancer in Northern Iran as a high‑risk region

Genetic and histological subtypes of gastric cancer reviewed, particularly emphasising on microsatellite instability and E-cadherin gene mutation

Association between ERCC5 gene polymorphisms and gastric cancer risk in a Chinese population

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