Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression

Detalhes bibliográficos
Autor(a) principal: Lima, Valeska Portela
Data de Publicação: 2008
Outros Autores: Lima, Marcos Antonio Pereira de, André, Ângela Rosa, Ferreira, Márcia Valéria Pitombeira, Barros, Marcos Aurélio Pessoa, Rabenhorst, Silvia Helena Barem
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da Universidade Federal do Ceará (UFC)
Texto Completo: http://www.repositorio.ufc.br/handle/riufc/5370
Resumo: AIM: To investigate the interrelationship between H 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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spelling Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expressionHelicobacter pyloriNeoplasis GátricasAIM: To investigate the interrelationship between H 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.OBJETIVO: Investigar a relação entre H pylori e vírus (EBV) Epstein-Barr na carcinogênese gástrica, tendo em foco a p53 mutação ea expressão de c-Myc, Bcl-2 e Bax. MÉTODOS: setenta e um tecidos de carcinoma gástrico foram avaliados pela reação em cadeia da polimerase (PCR) para H pylori e in situ hibridização para EBV. c-Myc, Bcl-2 e expressão do Bax foram detectados por imuno-histoquímica e de polimorfismo conformacional de cadeia simples (SSCP) para p53 mutação. RESULTADOS: As taxas de positividade para H. pylori e EBV foram de 94,4% e 8,45%, respectivamente. A maior parte dos casos, apresentada apenas a H. pylori presença. Todos os casos EBV positivos também foram H pylori positivo. Nenhum agente infeccioso foi observada em 5,55% dos casos. O tipo de tumor intestinal foi mais frequente nos grupos de co-infectados e não infectados. A fêmea predominou no grupo não infectado atingindo significância estatística (70,4% vs 29,6%, P = 0,039). A proteína Bcl-2 foi detectado apenas no grupo infectado exclusivamente por H. pylori . No entanto, c-Myc e Bax foram detectados nos três grupos, mas com uma frequência baixa no grupo co-infectados. A mutação do p53 esteve presente em todos os grupos, com as maiores freqüências nas H. pylori grupos positivos. CONCLUSÃO: A freqüência de H pylori infecção em carcinomas gástricos era alta. Os dados apresentados indicam que gástrico carcinogénese tem diferentes vias, dependendo da presença de dois agentes infecciosos investigados, sugerindo um possível envolvimento de H. pylori com o processo de apoptose. A baixa expressão de c-Myc e Bax nos grupos EBV positivos, sugere que o EBV podem inibir a expressão destas proteínas. No entanto, o p53 mutação mostra-se uma alteração relevante, independentemente de ambos os agentes infecciosos.World Journal of Gastroenterology2013-07-16T14:17:04Z2013-07-16T14:17:04Z2008-02info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfLIMA, V. P. et al. Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression. World Journal of Gastroenterology, v. 14, n. 6, p. 884-891, fev. 2008.1007-9327http://www.repositorio.ufc.br/handle/riufc/5370Lima, Valeska PortelaLima, Marcos Antonio Pereira deAndré, Ângela RosaFerreira, Márcia Valéria PitombeiraBarros, Marcos Aurélio PessoaRabenhorst, Silvia Helena Baremengreponame:Repositório Institucional da Universidade Federal do Ceará (UFC)instname:Universidade Federal do Ceará (UFC)instacron:UFCinfo:eu-repo/semantics/openAccess2022-05-20T13:43:12Zoai:repositorio.ufc.br:riufc/5370Repositório InstitucionalPUBhttp://www.repositorio.ufc.br/ri-oai/requestbu@ufc.br || repositorio@ufc.bropendoar:2024-09-11T19:00:50.798996Repositório Institucional da Universidade Federal do Ceará (UFC) - Universidade Federal do Ceará (UFC)false
dc.title.none.fl_str_mv Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
title Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
spellingShingle Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
Lima, Valeska Portela
Helicobacter pylori
Neoplasis Gátricas
title_short Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
title_full Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
title_fullStr Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
title_full_unstemmed Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
title_sort Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and bax expression
author Lima, Valeska Portela
author_facet Lima, Valeska Portela
Lima, Marcos Antonio Pereira de
André, Ângela Rosa
Ferreira, Márcia Valéria Pitombeira
Barros, Marcos Aurélio Pessoa
Rabenhorst, Silvia Helena Barem
author_role author
author2 Lima, Marcos Antonio Pereira de
André, Ângela Rosa
Ferreira, Márcia Valéria Pitombeira
Barros, Marcos Aurélio Pessoa
Rabenhorst, Silvia Helena Barem
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Lima, Valeska Portela
Lima, Marcos Antonio Pereira de
André, Ângela Rosa
Ferreira, Márcia Valéria Pitombeira
Barros, Marcos Aurélio Pessoa
Rabenhorst, Silvia Helena Barem
dc.subject.por.fl_str_mv Helicobacter pylori
Neoplasis Gátricas
topic Helicobacter pylori
Neoplasis Gátricas
description AIM: To investigate the interrelationship between H 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.
publishDate 2008
dc.date.none.fl_str_mv 2008-02
2013-07-16T14:17:04Z
2013-07-16T14:17:04Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv LIMA, V. P. et al. Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression. World Journal of Gastroenterology, v. 14, n. 6, p. 884-891, fev. 2008.
1007-9327
http://www.repositorio.ufc.br/handle/riufc/5370
identifier_str_mv LIMA, V. P. et al. Helicobacter pylori (CagA) and Epstein Barr virus infection in gastric carcinomas : correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression. World Journal of Gastroenterology, v. 14, n. 6, p. 884-891, fev. 2008.
1007-9327
url http://www.repositorio.ufc.br/handle/riufc/5370
dc.language.iso.fl_str_mv eng
language eng
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv World Journal of Gastroenterology
publisher.none.fl_str_mv World Journal of Gastroenterology
dc.source.none.fl_str_mv reponame:Repositório Institucional da Universidade Federal do Ceará (UFC)
instname:Universidade Federal do Ceará (UFC)
instacron:UFC
instname_str Universidade Federal do Ceará (UFC)
instacron_str UFC
institution UFC
reponame_str Repositório Institucional da Universidade Federal do Ceará (UFC)
collection Repositório Institucional da Universidade Federal do Ceará (UFC)
repository.name.fl_str_mv Repositório Institucional da Universidade Federal do Ceará (UFC) - Universidade Federal do Ceará (UFC)
repository.mail.fl_str_mv bu@ufc.br || repositorio@ufc.br
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