Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53

Detalhes bibliográficos
Autor(a) principal: Vieira, Antonia Catarine Gomes
Data de Publicação: 2022
Tipo de documento: Trabalho de conclusão de curso
Idioma: por
Título da fonte: Repositório Institucional da Universidade Federal do Ceará (UFC)
Texto Completo: http://www.repositorio.ufc.br/handle/riufc/69821
Resumo: Gastric cancer (GC) is the fifth most incident cancer and the fourth in mortality worldwide. The GC is extremely heterogeneous and among the molecules observed with alterations are the MYC and TP53 genes, involved with the cell cycle and apoptosis. Thus, the objective of this work was to investigate the relationship between the presence of H. pylori and the genotypes (cagA, cagE and vacA alleles), associated with the expression of TP53 and MYC. We studied 82 patients with GC. The presence of H. pylori and genotypes was performed using the PCR technique. MYC(+) overexpression and TP53(p53+) expression were detected by immunohistochemistry. H pylori infection was observed in 85.4% (70/82) of the cases, with vacAs1 being the most frequent genotype (87,1%; 61/70). The cagA and cagE genes were detected in 62.8% (44/70) and 54.3% (38/70) of cases, respectively. TP53(+) was detected in 28.6% (20/70), and MYC(+) at 36.6% (30/82) in the core; 6.1% (5/82) in the cytoplasm, and 7.3 (6/82) for co-localization. Comparative analyzes between the frequency of the genes studied or in combination showed that nuclear MYC positivity was significantly more frequent in diffuse tumors (50%; 18/36), showing approximately 2x risk of the MYC nuclear tumor developing the diffuse subtype [p=0.025; OR = 2.8 (1.01 - 7.96)]. In positive cases for H pylori, there was a risk tendency for the double-labelled MYCN(+)TP53(+) to develop the diffuse subtype [p=0.063; OR: 5.35 (0.63-65.33)]. In addition, cagA positive strains and the presence of nuclear MYC were significantly more frequent in diffuse tumors (10/17; 58,8%), were approximately 8x more likely to develop this subtype [p=0,006; OR = 8,21 (1,62 – 45,52)]. The results indicate that, in diffuse tumors, a carcinogenic pathway associated with TP53 expression, and possibly influenced by H pylori cagA(+), seems to occur probably through the MYC protein.
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spelling Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53Adenocarcinoma gástricoHelicobacter pyloriMYCTP53Gastric cancer (GC) is the fifth most incident cancer and the fourth in mortality worldwide. The GC is extremely heterogeneous and among the molecules observed with alterations are the MYC and TP53 genes, involved with the cell cycle and apoptosis. Thus, the objective of this work was to investigate the relationship between the presence of H. pylori and the genotypes (cagA, cagE and vacA alleles), associated with the expression of TP53 and MYC. We studied 82 patients with GC. The presence of H. pylori and genotypes was performed using the PCR technique. MYC(+) overexpression and TP53(p53+) expression were detected by immunohistochemistry. H pylori infection was observed in 85.4% (70/82) of the cases, with vacAs1 being the most frequent genotype (87,1%; 61/70). The cagA and cagE genes were detected in 62.8% (44/70) and 54.3% (38/70) of cases, respectively. TP53(+) was detected in 28.6% (20/70), and MYC(+) at 36.6% (30/82) in the core; 6.1% (5/82) in the cytoplasm, and 7.3 (6/82) for co-localization. Comparative analyzes between the frequency of the genes studied or in combination showed that nuclear MYC positivity was significantly more frequent in diffuse tumors (50%; 18/36), showing approximately 2x risk of the MYC nuclear tumor developing the diffuse subtype [p=0.025; OR = 2.8 (1.01 - 7.96)]. In positive cases for H pylori, there was a risk tendency for the double-labelled MYCN(+)TP53(+) to develop the diffuse subtype [p=0.063; OR: 5.35 (0.63-65.33)]. In addition, cagA positive strains and the presence of nuclear MYC were significantly more frequent in diffuse tumors (10/17; 58,8%), were approximately 8x more likely to develop this subtype [p=0,006; OR = 8,21 (1,62 – 45,52)]. The results indicate that, in diffuse tumors, a carcinogenic pathway associated with TP53 expression, and possibly influenced by H pylori cagA(+), seems to occur probably through the MYC protein.O câncer gástrico (CG) é o quinto câncer mais incidente e o quarto em mortalidade no mundo. O CG é extremamente heterogêneo e entre as a moléculas observadas com alterações encontra-se os genes MYC e TP53, envolvidos com o ciclo celular e apoptose. Assim, o objetivo deste trabalho foi investigar a relação entre presença de H. pylori e genótipos (cagA, cagE e alelos vacA), associando com a expressão de TP53 e de MYC. Foram estudados 82 pacientes com CG. A presença de H. pylori e genótipos foi realizada pela técnica de PCR. A superexpressão de MYC(+) e a expressão de TP53(p53+) foi detectada por imuno-histoquímica. A infecção por H. pylori foi observada em 85,4% (70/82) dos casos, sendo a vacAs1 o genótipo mais frequente (87,1%; 61/70). Os genes cagA e cagE foram detectados em 62,8% (44/70) e 54,3% (38/70) dos casos respectivamente. TP53(+) foi detectada em 28,6% (20/70), e MYC(+) em 36,6% (30/82) no núcleo; 6,1% (5/82) no citoplasma, e 7,3 (6/82) para co-localização. As análises comparativas entre a frequência dos genes estudados ou em combinação mostraram que a positividade de MYC nuclear foi significativamente mais frequente nos tumores difusos (50%; 18/36), mostrando risco de aproximadamente 2x do tumor MYC nuclear desenvolver o subtipo difuso [p=0,025; OR = 2,8 (1,01 – 7,96)]. Nos casos H. pylori positivos, observou-se uma tendência ao risco para a dupla marcação MYCN(+)TP53(+) desenvolver o subtipo difuso [p=0,063; OR: 5,35 (0,63-65,33)]. Além disso, cepas cagA positivas e a presença de MYC nuclear form significativamente mais frequente nos tumores difusos (10/17; 58,8%), apresentaram risco aproximadamente 8x maior para o desenvolvimento desse subtipo [p=0,006; OR = 8,21 (1,62 – 45,52)]. Os resultados indicam que, nos tumores difusos a via carcinogênica associada à expressão de TP53, e possivelmente influenciada por H. pylori cagA(+), parece ocorrer provavelmente por meio da proteína MYC.Rabenhorst, Silvia Helena BaremVieira, Antonia Catarine Gomes2022-12-20T16:55:15Z2022-12-20T16:55:15Z2022info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/bachelorThesisapplication/pdfVIEIRA, Antonia Catarine Gomes. Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53. 2022. 51 f. Trabalho de conclusão de curso (Graduação em Ciências Biológicas) – Centro de Ciências, Universidade Federal do Ceará, Fortaleza, 2022.http://www.repositorio.ufc.br/handle/riufc/69821porreponame:Repositório Institucional da Universidade Federal do Ceará (UFC)instname:Universidade Federal do Ceará (UFC)instacron:UFCinfo:eu-repo/semantics/openAccess2022-12-20T16:55:34Zoai:repositorio.ufc.br:riufc/69821Repositório InstitucionalPUBhttp://www.repositorio.ufc.br/ri-oai/requestbu@ufc.br || repositorio@ufc.bropendoar:2024-09-11T18:16:37.684234Repositório Institucional da Universidade Federal do Ceará (UFC) - Universidade Federal do Ceará (UFC)false
dc.title.none.fl_str_mv Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
title Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
spellingShingle Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
Vieira, Antonia Catarine Gomes
Adenocarcinoma gástrico
Helicobacter pylori
MYC
TP53
title_short Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
title_full Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
title_fullStr Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
title_full_unstemmed Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
title_sort Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53
author Vieira, Antonia Catarine Gomes
author_facet Vieira, Antonia Catarine Gomes
author_role author
dc.contributor.none.fl_str_mv Rabenhorst, Silvia Helena Barem
dc.contributor.author.fl_str_mv Vieira, Antonia Catarine Gomes
dc.subject.por.fl_str_mv Adenocarcinoma gástrico
Helicobacter pylori
MYC
TP53
topic Adenocarcinoma gástrico
Helicobacter pylori
MYC
TP53
description Gastric cancer (GC) is the fifth most incident cancer and the fourth in mortality worldwide. The GC is extremely heterogeneous and among the molecules observed with alterations are the MYC and TP53 genes, involved with the cell cycle and apoptosis. Thus, the objective of this work was to investigate the relationship between the presence of H. pylori and the genotypes (cagA, cagE and vacA alleles), associated with the expression of TP53 and MYC. We studied 82 patients with GC. The presence of H. pylori and genotypes was performed using the PCR technique. MYC(+) overexpression and TP53(p53+) expression were detected by immunohistochemistry. H pylori infection was observed in 85.4% (70/82) of the cases, with vacAs1 being the most frequent genotype (87,1%; 61/70). The cagA and cagE genes were detected in 62.8% (44/70) and 54.3% (38/70) of cases, respectively. TP53(+) was detected in 28.6% (20/70), and MYC(+) at 36.6% (30/82) in the core; 6.1% (5/82) in the cytoplasm, and 7.3 (6/82) for co-localization. Comparative analyzes between the frequency of the genes studied or in combination showed that nuclear MYC positivity was significantly more frequent in diffuse tumors (50%; 18/36), showing approximately 2x risk of the MYC nuclear tumor developing the diffuse subtype [p=0.025; OR = 2.8 (1.01 - 7.96)]. In positive cases for H pylori, there was a risk tendency for the double-labelled MYCN(+)TP53(+) to develop the diffuse subtype [p=0.063; OR: 5.35 (0.63-65.33)]. In addition, cagA positive strains and the presence of nuclear MYC were significantly more frequent in diffuse tumors (10/17; 58,8%), were approximately 8x more likely to develop this subtype [p=0,006; OR = 8,21 (1,62 – 45,52)]. The results indicate that, in diffuse tumors, a carcinogenic pathway associated with TP53 expression, and possibly influenced by H pylori cagA(+), seems to occur probably through the MYC protein.
publishDate 2022
dc.date.none.fl_str_mv 2022-12-20T16:55:15Z
2022-12-20T16:55:15Z
2022
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/bachelorThesis
format bachelorThesis
status_str publishedVersion
dc.identifier.uri.fl_str_mv VIEIRA, Antonia Catarine Gomes. Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53. 2022. 51 f. Trabalho de conclusão de curso (Graduação em Ciências Biológicas) – Centro de Ciências, Universidade Federal do Ceará, Fortaleza, 2022.
http://www.repositorio.ufc.br/handle/riufc/69821
identifier_str_mv VIEIRA, Antonia Catarine Gomes. Influência da infecção por H. Pylori nas Vias Carcinogênicas Gástricas envolvendo os genes MYC e TP53. 2022. 51 f. Trabalho de conclusão de curso (Graduação em Ciências Biológicas) – Centro de Ciências, Universidade Federal do Ceará, Fortaleza, 2022.
url http://www.repositorio.ufc.br/handle/riufc/69821
dc.language.iso.fl_str_mv por
language por
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
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dc.format.none.fl_str_mv application/pdf
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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