Expression of mutant type-<i>p</i>53 products in<i>H pylori</i>-associated chronic gastritis

Kodama, Masaaki; Murakami, Kazunari; Okimoto, Tadayoshi; Sato, Ryugo; Watanabe, Koichiro; Fujioka, Toshio

doi:10.3748/wjg.v13.i10.1541

Cited by 31 publications

(22 citation statements)

References 26 publications

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“…The present study shows the highest frequency of p53 mutation in the groups with H pylori infection, especially among the cagA+ cases, corroborating previous studies [16,3,4] . The high percentage of p53 mutation in EBV-associated and EBV-negative gastric carcinomas was observed in our study which was also demonstrated in other studies, demonstrating that the p53 mutation is a relevant alteration in gastric carcinogenesis independent of the infection [15,16,43] . Finally, this study shows the high prevalence of H pylori infection in gastric carcinomas in Ceará State.…”

Section: Discussionsupporting

confidence: 90%

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H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

Lima

Lima²,

André³

et al. 2008

WJG

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AIM: To investigate the interrelationship betweenH pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression.METHODS: seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation. RESULTS:The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P = 0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori .However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups. CONCLUSION:The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.

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Section: Discussionsupporting

confidence: 90%

“…Kodama et al [43] have suggested an accumulation of wild-type p53, especially in the H pylori infected mucosa probably due to the H pylori-induced DNA damage. The present study shows the highest frequency of p53 mutation in the groups with H pylori infection, especially among the cagA+ cases, corroborating previous studies [16,3,4] .…”

Section: Discussionmentioning

confidence: 99%

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

Lima

Lima²,

André³

et al. 2008

WJG

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“…Previous studies have indicated that over-expression of p53 protein detected by immunohistochemistry generally represents mutant p53 (Nardone et al 1999;Murakami et al 1999;Kodama et al 2007), suggesting that the immunochistochemical accumulation of p53 is an indicator of the loss of the p53 tumor suppressor function. Therefore, the p53 protein accumulation detected in non-acid-secreting areas might represent important molecular events involved in the persistent gastric carcinogenesis after H. pylori eradication.…”

Section: Discussionmentioning

confidence: 98%

“…It has been reported that immunohistochemical accumulation of p53 was found in gastric mucosa infected with H. pylori infection and that it significantly decreased after eradication (Jones et al 1997;Nardone et al 1999;Satoh et al 2001;Kodama et al 2007). On the other hand, another study pointed out that significantly higher accumulation of p53 was detected in the gastric mucosa of patients with multifocal atrophic gastritis 1 year after eradication compared with that of patients with non-atrophic superficial gastritis (Guarner et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

Iijima

Abe

Koike

et al. 2012

Tohoku J. Exp. Med.

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Although Helicobacter pylori (H. pylori) eradication has some inhibitory effects on the subsequent development of gastric cancer, there are sporadic cases of gastric cancer even after successful eradication. The pathogenesis of gastric cancer emerging after H. pylori eradication remains to be clarified. In this study, employing Congo-red chromoendoscopy, which is capable of visualizing the acid-secreting fundic mucosa, we investigated the topographic relationship of the acid secretion pattern to the occurrence site of gastric cancers emerging after eradication. Fourteen consecutive patients who suffered from new gastric cancer after eradication, defined as lesions that were discovered at least 2 years after the eradication, were prospectively enrolled. Whether the neoplasias arose from acid-secreting or nonacid-secreting areas was evaluated with Congo-red chromoendoscopy. Biopsy specimens taken from the two areas were subjected to histologic evaluation and immunohistochemistry for Ki-67 and p53. The mean period from the eradication to the subsequent occurrence of gastric cancer was 74 (44) months. There were two cancer lesions in 5 cases, and thus there was a total 19 lesions from 14 cases. Congo-red chromoendoscopy revealed that all 19 lesions arose exclusively from non-acid-secreting areas. Histological examination revealed sustained hyperproliferation and accumulation of p53 protein was frequently detectable in non-acid-secreting areas. Genetic alteration such as p53 mutation seems to be already present in the residual non-acid-secreting areas after eradication, areas that could be the origin of gastric carcinogenesis after eradication. Identification of such high-risk areas should be a promising approach for estimating the individual cancer risk after eradication.

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“…Several studies have shown that the detection of p53 in the presence of lowgrade dysplasia is a risk factor for progression to highgrade dysplasia or cancer. Thus it is expected that p53 mutation status causes the mutant type of p53 expression [19,20]. However, no correlation was found between p53 mutation analysis and immunohistochemical staining in H. pylori-associated gastroduodenal diseases including GC.…”

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confidence: 99%

A study on the effect of Helicobacter pylori infection on p53 expression in gastric cancer and gastritis tissues

Salih

Güçin

Bayyurt

2013

J Infect Dev Ctries

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Introduction: Helicobacter pylori cause damage to gastric epithelial cells and alterations in the p53 gene that lead to cancer development. This study aimed to determine the correlation of p53 expression with H. pylori using immunohistochemistry, RFLP-PCR, and histopathology. Methodology: Gastric biopsy samples from gastric cancer (GC) (n = 54) and gastritis (n = 31) patients were examined for histopathological changes and expression of p53 protein by immunohistochemistry. Results: Immunohistochemical analysis of p53 protein expression in H. pylori-positive GC sections showed an average of 44.3% positive cells in tumors and 6.9% in normal tissues, as compared to 16.4% and 4.4% in H. pylori-negative sections. P53 expression showed significant association with H. pylori (P = 0.005), invasion depth (P = 0.029) and inflammation reaction (P = 0.008). In gastritis sections, no difference in the average p53 staining in H. pylori-positive or -negative sections was seen. PCR-RFLP results also showed no difference in genotype frequencies of p53 in H. pylori-positive or -negative gastritis sections. Histopathology study of H. pylori-positive GC sections showed that 97.2% were the intestinal type and 2.8% the diffuse type, while in H. pylori-negative sections 35.2% were the intestinal type and 64.8% the diffuse type. Biopsy sections from H. pylori-positive gastritis patients revealed more severe inflammation than those of H. pylorinegative patients. Conclusion: Our results show that H. pylori infection affects p53 expression in GC. The average p53 expression was significantly higher in tumor than in normal tissues. In gastritis sections p53 expression was significantly associated with H. pylori.

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Expression of mutant type-p53 products inH pylori-associated chronic gastritis

Abstract: AIM:To investigate the mutation of p 53 immunohistochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.

Cited by 31 publications

References 26 publications

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

A study on the effect of Helicobacter pylori infection on p53 expression in gastric cancer and gastritis tissues

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