<i>Helicobacter pylori</i>infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

Zhang, Chuan; Yamada, Nobutaka; Wu, Ying; Wen, Min; Matsuhisa, Takeshi; Matsukura, Norio

doi:10.3748/wjg.v11.i6.791

Cited by 117 publications

(112 citation statements)

References 35 publications

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“…In our study, the rate of H. pylori infection was lower in GC cases (60.4%), compared with those in SG (85.0%) and AG (87.7%) cases. Our findings were similar to those obtained in a Chinese study which showed that whereas the rates were 63.3% and 80.8%, respectively, in gastric erosion and gastric ulcer, the overall rate was 52.4% in patients with early gastric cancer, with the rates being 35.0%, 50.7%, 34.6%, respectively, in the antrum, corpus, and incisura of stomach (Zhang et al, 2005). Indeed, it has been shown that development of precancerous and cancerous lesions may create a hostile environment to H. pylori, and thus H. pylori infection may disappear following the development of these lesions (Genta et al, 1993).…”

Section: 215 Wnt Pathway Expression and Hpylori Infection In Gastrisupporting

confidence: 79%

Expression of the E-cadherin/β-catenin/tcf-4 Pathway in Gastric Diseases with Relation to Helicobacter pylori Infection: Clinical and Pathological Implications

Yu¹,

Xu²,

Xu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Objective: To determine the expression of E-cadherin, β-catenin, and transcription factor 4 (TCF4) proteins in gastric diseases with relation to Helicobacter pylori infection. Methods: A total of 309 patients including 60 with superficial gastritis (SG), 57 with atrophic gastritis (AG) and 192 with gastric cancer (GC), were enrolled. The expression of E-cadherin, β-catenin, TCF4 proteins in the gastric mucosa was detected by immunohistochemistry and H. pylori infection by immunohistochemistry and PCR. Results: The expression rates of E-cadherin were significantly higher in SG and AG than in GC (P<0.01), while those of β-catenin in the nucleus were significantly lower in SG and AG than in GC (P<0.05). In GC cases, the expression rates of E-cadherin, β-catenin and TCF4 were significantly higher in the intestinal type than in the diffuse type (P<0.05). In GC patients, the expression rate of E-cadherin was significantly higher in the presence of H. pylori than in the absence of infection (P=0.011). Moreover, the expression level of TCF4 and β-catenin protein was significantly higher in the nucleus and cytoplasm in H. pylori positive than in H. pylori negative GC patients, especially in those with the intestinal type (all P < 0.05). Conclusion: The expression of E-cadherin and β-catenin progressively decreases during the process of GC tumorigenesis, while overexpression of TCF4 occurs. H. pylori infection is associated with a significant increase in the expression of E-cadherin and β-catenin in the cytoplasm and nucleus in GC patients, especially those with the intestinal type.

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Section: 215 Wnt Pathway Expression and Hpylori Infection In Gastrisupporting

confidence: 79%

Expression of the E-cadherin/β-catenin/tcf-4 Pathway in Gastric Diseases with Relation to Helicobacter pylori Infection: Clinical and Pathological Implications

Yu¹,

Xu²,

Xu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…O adenocarcinoma gástrico atinge altas taxas de incidência em países orientais como China e Japão, especialmente quando comparadas com as taxas encontradas no ocidente. UEMURA et al (41) (11,44,45) .…”

Section: Resultsunclassified

“…A significância estatística foi obtida através do teste do qui-quadrado, com intervalo de confiança de 95%. v. 44 …”

Section: Métodosunclassified

Prevalência da infecção por Helicobacter pylori e das lesões precusoras do câncer gástrico em pacientes dispéticos

Müller

Fagundes

Moraes

et al. 2007

Arq. Gastroenterol.

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RESUMO -Racional -A infecção pelo Helicobacter pylori é fator importante no desenvolvimento da carcinogênese gástrica, mas somente uma fração dos pacientes infectados irá desenvolver câncer gástrico. A infecção pelo H. pylori determina gastrite crônica não-atrófica, que pode evoluir para gastrite atrófica e metaplasia intestinal e, finalmente, para displasia e adenocarcinoma. , 3% e 15% das biopsias, respectivamente. A infecção por H. pylori determinou uma razão de chances 10 vezes (IC95% 6.50 -17%) maior de se encontrar algum grau de alteração histológica na mucosa gástrica. A razão de chances dos pacientes infectados apresentarem gastrite crônica não-atrófica, foi igual a 3 (IC95% 2,2 -3,4). A razão de chances dos pacientes infectados apresentarem gastrite atrófica e metaplasia intestinal foi menor que 1. Conclusão -A prevalência da infecção por H. pylori foi alta (76%) e os indivíduos infectados apresentaram probabilidade 10 vezes maior para a ocorrência de lesão da mucosa gástrica. Gastrite crônica não-atrófica apresentou prevalência de 77%, gastrite atrófica 3% e metaplasia intestinal 15%. A infecção pelo H. pylori determinou uma probabilidade 3 vezes maior para o desenvolvimento de gastrite crônica não-atrófica e não determinou risco para a ocorrência de gastrite atrófica e metaplasia intestinal, sugerindo que possivelmente outros fatores de risco, além do H. pylori, estejam envolvidos no processo da carcinogênese gástrica. DESCRITORES -Infecções por Helicobacter. Neoplasias gástricas. Condições pré-cancerosas. Dispepsia. INTRODUÇÃOO câncer gástrico é a segunda causa mais comum de morte por câncer no mundo e quase dois terços dos casos ocorrem em países em desenvolvimento (28) . Progresso significante na etiologia do câncer gástrico foi a identificação do Helicobacter pylori (H. pylori) e as evidências acumuladas que levaram a sua classificação como fator importante ligado ao processo da carcinogênese gástrica. No entanto, tem-se observado grande heterogeneidade entre as populações, no que diz respeito ao risco do desenvolvimento de câncer gástrico associado à infecção pelo H. pylori, notando-se que nas populações com alta prevalência da infecção somente uma fração da mesma irá desenvolver câncer gástrico (15) .Estudos da mucosa gástrica em populações de alto risco têm revelado uma série de lesões que, seqüencialmente, evoluiriam da condição normal para gastrite crônica não-atrófica (GCNA), que evoluiria para gastrite atrófica (GA) e metaplasia intestinal (MI) e, finalmente, para displasia e adenocarcinoma (7,8,10,35) . Portanto, a infecção pelo

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“…Furthermore, the prevalence rate of gastric cancer has decreased each year [6]. In addition, half of the patients with early gastric cancer are negative for H. pylori antibody [7].…”

Section: Introductionmentioning

confidence: 99%

Long-term administration of the fungus toxin, sterigmatocystin, induces intestinal metaplasia and increases the proliferative activity of PCNA, p53, and MDM2 in the gastric mucosa of aged Mongolian gerbils

Kusunoki

Misumi

Shimada

et al. 2011

Environ Health Prev Med

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Objective The causal agents of gastric cancer could include fungus toxins. Sterigmatocystin (ST), a fungus toxin, is a risk factor of gastric cancer. We investigated the effects of ST on the stomach tissues of Mongolian gerbils. Methods Seventy-five-week-old male Mongolian gerbils received ST ad libitum at a concentration of 0 ppb (nontreated, n = 11), 100 ppb (n = 7), or 1,000 ppb (n = 13) dissolved in drinking water for a period of 24 weeks. After administration, we tested the histopathological changes and immunostaining for proliferating cell nuclear antigen (PCNA), p53, and MDM2 expression. Results We investigated the histopathological changes and determined the incidence of histopathological changes in animals with various gastric diseases after ST administration at a dose of 0 ppb (non-treated control), 100, or 1,000 ppb as follows: firstly, indices for gastritis were 18.2, 100, and 100%, those for erosion events were 9.1, 100, and 92.3%, and those for polyps were 0, 71.4, and 61.5%, respectively. These incidences in the ST-administered groups (100 or 1,000 ppb) showed significant increases compared with those in the non-treated control group. And, lastly, indices for intestinal metaplasia were 0, 100, and 15.4%, respectively. Furthermore, immunostaining for PCNA, p53, and MDM2 expression showed significantly greater rates in the ST-administered groups (100 or 1,000 ppb) than in the non-treated control group. Conclusion The histopathological and immunohistopathological findings of this study indicate that ST exerts a marked influence on gastric mucus and gland cells, showing dominant gastritis, erosion events, polyps, and intestinal metaplasia in these animals.

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Helicobacter pyloriinfection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

Cited by 117 publications

References 35 publications

Expression of the E-cadherin/β-catenin/tcf-4 Pathway in Gastric Diseases with Relation to Helicobacter pylori Infection: Clinical and Pathological Implications

Expression of the E-cadherin/β-catenin/tcf-4 Pathway in Gastric Diseases with Relation to Helicobacter pylori Infection: Clinical and Pathological Implications

Prevalência da infecção por Helicobacter pylori e das lesões precusoras do câncer gástrico em pacientes dispéticos

Long-term administration of the fungus toxin, sterigmatocystin, induces intestinal metaplasia and increases the proliferative activity of PCNA, p53, and MDM2 in the gastric mucosa of aged Mongolian gerbils

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