The role of the HLA-DQA1 gene in resistance to atrophic gastritis and gastric adenocarcinoma induced byHelicobacter pylori infection

Azuma, Takeshi; Ito, Shigeji; Sato, Fukiko; Yamazaki, Yukinao; Miyaji, Hideki; Ito, Yoshiyuki; Suto, Hiroyuki; Kuriyama, Masaru; Kato, Takuji; Kohli, Yoshihiro

doi:10.1002/(sici)1097-0142(19980315)82:6<1013::aid-cncr2>3.0.co;2-f

Cited by 117 publications

(78 citation statements)

References 28 publications

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“…They found that the allele frequency of DQA1 was significantly lower in H. pylori positive atrophic gastritis group than in H. pylori positive superficial gastritis and normal control groups. In addition, the al lele frequency of DQA1 also was significantly lower in H. pylori positive intestinal type gastric adenocarcinoma group than in normal control, H. pylori positive superficial gastritis, and diffuse type gastric adenocarcinoma groups [69] . The importance of host genetic factors in determining the outcome of H. pylori infection was further demonstrated by Sakagami and colleagues.…”

Section: Host Genetic Factorsmentioning

confidence: 81%

Molecular mechanisms ofH. pyloriassociated gastric carcinogenesis

Zhang¹,

Farthing²

1999

WJG

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Section: Host Genetic Factorsmentioning

confidence: 81%

Molecular mechanisms ofH. pyloriassociated gastric carcinogenesis

Zhang¹,

Farthing²

1999

WJG

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“…26 Absence of HLA-DQA1 0101 may be a host genetic risk factor for H. pylori-associated atrophic gastritis and for intestinal-type gastric adenocarcinoma. 27 Lewis antigen and secreted phenotype have been related to the attachment of H. pylori to gastric mucosa and subsequent epithelial damage. 28 It has been reported that anomalous Lewis antigen (a) expression in Lewis (a-bϩ) phenotype individuals was closely related to the severity of the histologic lesions, especially to dysplasia and type III intestinal metaplasia.…”

Section: Discussionmentioning

confidence: 99%

Role of Helicobacter pylori infection among offspring or siblings of gastric cancer patients

Chang

Han

Lee

et al. 2002

Intl Journal of Cancer

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A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. Gastric cancer is the second most common cause of cancerrelated death in the world. 1 In Korea, gastric cancer is the most frequently diagnosed malignancy, although the associated mortality rate has been decreasing slowly for the past 10 years. 2 About 60% of Korean adults are infected with Helicobacter pylori. 3,4 Such infection is a causative factor in gastric carcinogenesis, and H. pylori infection is associated with a 2-fold increased risk of developing gastric adenocarcinoma. 5,6 A positive family history is also associated with an increased risk of gastric cancer. 7-10 The possible causes of familial aggregation of gastric cancer are common genetic backgrounds and common environmental risk factors including H. pylori infection, excessive intake of salt and N-nitroso compounds and a deficiency of dietary antioxidants among patients with gastric cancer and their family members. Among these risk factors, intrafamilial clustering of H. pylori infection is regarded as a leading cause of gastric carcinogenesis. This association is significantly greater for H. pylori strains that possess the cytotoxin-associated gene cagA, [11][12][13] a key gene of the so-called "pathogenicity island". 14 The first aim of our study was to examine the prevalence of H. pylori infection in offspring and siblings of patients with gastric cancer to evaluate its role in intrafamilial aggregation of gastric cancer. The second aim was to investigate the relationship between CagA or vacuolating cytotoxin (VacA) seropositivity as virulence markers of H. pylori strains and H. pylori infection in relatives of cancer patients. Finally, we examined the frequency of gastric precancerous lesion, atrophic gastritis and/or intestinal metaplasia in the H. pyloriinfected relatives of cancer patients. MATERIAL AND METHODS Recruitment of relatives of cancer patients and controlsFrom November 2000 to March 2002, we recruited subjects who wished to receive routine upper gastrointestinal endoscopy and evaluation ...

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“…At the expected false significance rate of 0.88%, 54 up-regulated and 471 down-regulated genes were detected in colon polyps compared to normal mucosa crypts. gastritis and gastric cancer (33), although the pathobiological role in colon carcinogenesis is not clear.…”

Section: Fcgbp Slc26a2 Eplin Tspan1 Pdcd4 Pex1 Mtus1 Fabp1 Ddmentioning

confidence: 99%

Differential expression in normal-adenoma-carcinoma sequence suggests complex molecular carcinogenesis in colon

Lee

Bang²,

Song³

et al. 2006

Oncol Rep

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Abstract. The majority of colon cancers develop from preexisting adenomas. We analyzed the expression profiles in the sequence of normal colon crypts, adenomas and earlystage carcinomas using microdissected cells from tubular adenomas with foci of malignant transformation. Differentially expressed genes were detected between normal-adenoma and adenoma-carcinoma, and were grouped according to the patterns of expression changes in the sequence. Down-regulated genes in the sequence included PLA2G2A, TSPAN1, PDCD4, FCGBP, AATK, EPLIN, FABP1, AGR2, MTUS1, TSC1, galectin 4 and MT1F. PLA2G2A has been shown to suppress colon tumorigenesis in mice, but the pathobiological role in humans has been controversial. Our data showed continuous down-regulation of PLA2G2A in the sequence supporting an implication in human colon cancer. Tumor suppressor and/ or proapoptotic activities have also been reported in other genes. Up-regulated genes included ribosomal proteins, IER3 and TPR. TGF-ß2 and matrix metalloproteinase 23B were up-regulated in carcinoma but not in adenoma, supporting the pathobiological roles in malignant transformation. Differentially expressed genes partly coincided with those in the adenoma-carcinoma sequence of the stomach, which was published previously, suggesting a partial overlap between the adenoma-carcinoma sequences of the colon and stomach.

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The role of the HLA-DQA1 gene in resistance to atrophic gastritis and gastric adenocarcinoma induced byHelicobacter pylori infection

Abstract: RESULTS. Of 70 -90% of patients with gastric adenocarcinoma. The epidemiologic features of gastric adenocarcinoma and H. pylori infection are similar,

Cited by 117 publications

References 28 publications

Molecular mechanisms ofH. pyloriassociated gastric carcinogenesis

Molecular mechanisms ofH. pyloriassociated gastric carcinogenesis

Role of Helicobacter pylori infection among offspring or siblings of gastric cancer patients

Differential expression in normal-adenoma-carcinoma sequence suggests complex molecular carcinogenesis in colon

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