How does<i>Helicobacter pylori</i>cause gastric cancer through connexins: An opinion review

Li, Huan; Xu, Canxia; Gong, Rui; Chi, Jingshu; Liu, Peng; Liu, Xiaoming

doi:10.3748/wjg.v25.i35.5220

Cited by 13 publications

(6 citation statements)

References 180 publications

(148 reference statements)

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“…Proteínas del huésped entre ellos algunos miembros de las conexinas (Cx) como son Cx26, Cx32, Cx37 y Cx34 tienen asociación con cáncer gástrico, los cambios de expresión de las conexinas inducidos por la bacteria están involucrados en la metástasis, invasión y apoptosis de las células (Li et al, 2019). Otro mecanismo de patogenicidad empleado por H. pylori es la metilación aberrante de ADN, muchos estudios demuestran que varias vías de producción del cáncer se relacionan con la metilación aberrante de ADN más que con mutaciones (Maeda et al, 2017).…”

Section: Resultados Y Discusiónunclassified

Helicobacter pylori y cáncer gástrico

et al. 2022

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Desde su descubrimiento Helicobacter pylori (H. Pylori) ha sido ampliamente estudiado y se ha encontrado asociado a niveles socioeconómicos bajos donde la prevalencia es mayor. Este microorganismo está involucrado en un amplio espectro de patología gástrica como: gastritis crónica, úlceras pépticas, adenocarcinoma y linfoma. En la actualidad se acepta el rol etiológico importante de H. pylori en el cáncer gástrico y sus lesiones precursoras, por lo que consideramos importante actualizar información sobre esta temática. Objetivo: Determinar el rol del Helicobacter pylori en el cáncer gástrico y sus lesiones precursoras, a través de la búsqueda bibliográfica en revistas científicas de los últimos 5 años. Métodos: Es un estudio descriptivo, retrospectivo, basado en la obtención de información documental sistemática de investigaciones realizadas en diferentes partes del mundo. Se recurrió a las siguientes bases de datos ScIELO, Science Direct y Google Académico, se seleccionaron artículos en inglés y en español. Resultados: Se seleccionaron 25 estudios publicados entre el 2015 y 2020 con los cuales se pudo dar cumplimiento al objetivo planteado. Conclusiones: H. pylori se encuentra involucrado en la génesis del cáncer gástrico y otras patologías gastrointestinales como la gastritis crónica, úlceras y linfoma MALT. Su prevalencia es mayor en países en vías de desarrollo que en países desarrollados. Emplea mecanismos patogénicos que le permiten colonizar la mucosa gástrica y producir una serie de alteraciones morfológicas que secuencialmente van desde la gastritis crónica, atrofia, metaplasia, displasia y adenocarcinoma.

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Section: Resultados Y Discusiónunclassified

Helicobacter pylori y cáncer gástrico

et al. 2022

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“…A decrease in OS and DFS in patients with moderate and marked concentrations of H. pylori coccoid forms in the GM may be due to the fact that these patients had more advanced stages and more aggressive forms of GC. Meanwhile, there are more and more studies showing that H. pylori infection can promote GC progression by activating the NF-κB signaling pathway and induction of interleukin-8 secretion[ 70 ], the activation of epithelial-mesenchymal transformation[ 71 - 74 ] and angiogenesis[ 75 , 76 ], as well as increasing the invasive properties of tumor cells[ 77 ]. It can be assumed that the administration of AT before surgery contributes to the reduction of the inflammatory process activity and normalization of the adhesive properties of tumour cells, which in turn decreases metastasis risk and improves the long-term results of the treatment of GC.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori in gastric cancer: Features of infection and their correlations with long-term results of treatment

Сеньчукова¹,

Tomchuk²,

Shurygina³

2021

WJG

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BACKGROUND Helicobacter pylori ( H. pylori ) is a spiral-shaped bacterium responsible for the development of chronic gastritis, gastric ulcer, gastric cancer (GC), and MALT-lymphoma of the stomach. H. pylori can be present in the gastric mucosa (GM) in both spiral and coccoid forms. However, it is not known whether the severity of GM contamination by various vegetative forms of H. pylori is associated with clinical and morphological characteristics and long-term results of GC treatment. AIM To establish the features of H. pylori infection in patients with GC and their correlations with clinical and morphological characteristics of diseases and long-term results of treatment. METHODS Of 109 patients with GC were included in a prospective cohort study. H. pylori in the GM and tumor was determined by rapid urease test and by immunohistochemically using the antibody to H. pylori . The results obtained were compared with the clinical and morphological characteristics and prognosis of GC. Statistical analysis was performed using the Statistica 10.0 software. RESULTS H. pylori was detected in the adjacent to the tumor GM in 84.5% of cases, of which a high degree of contamination was noted in 50.4% of the samples. Coccoid forms of H. pylori were detected in 93.4% of infected patients, and only coccoid-in 68.9%. It was found that a high degree of GM contamination by the coccoid forms of H. pylori was observed significantly more often in diffuse type of GC ( P = 0.024), in poorly differentiated GC ( P = 0.011), in stage T3-4 ( P = 0.04) and in N1 ( P = 0.011). In cases of moderate and marked concentrations of H. pylori in GM, a decrease in 10-year relapse free and overall survival from 55.6% to 26.3% was observed ( P = 0.02 and P = 0.07, respectively). The relationship between the severity of the GM contamination by the spiral-shaped forms of H. pylori and the clinical and morphological characteristics and prognosis of GC was not revealed. CONCLUSION The data obtained indicates that H. pylori may be associated not only with induction but also with the progression of GC.

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“…Additionally, gastric carcinogenesis can occur after H. pylori infection through the regulation of connexins (Cxs). This bacterium can upregulate transcription factors like GATA-3 and PBX-1, having a role in the expression of Cx32, which is thus inhibited [ 43 ]. In addition, it can decrease histone acetylation levels which in turn regulates the expression of Cxs.…”

Section: Gastric Carcinogenesismentioning

confidence: 99%

“…In addition, it can decrease histone acetylation levels which in turn regulates the expression of Cxs. Similarly, H. pylori modulates other connexins such as Cx43, Cx26 and Cx37, expressed in gastric tissue, either by promoter hypermethylation and expression inhibition, protein delocalisation or gene polymorphism induction [ 43 ].…”

Section: Gastric Carcinogenesismentioning

confidence: 99%

Gastric Cancer: Advances in Carcinogenesis Research and New Therapeutic Strategies

Seeneevassen

Bessède

Mégraud

et al. 2021

IJMS

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Gastric cancer’s bad incidence, prognosis, cellular and molecular heterogeneity amongst others make this disease a major health issue worldwide. Understanding this affliction is a priority for proper patients’ management and for the development of efficient therapeutical strategies. This review gives an overview of major scientific advances, made during the past 5-years, to improve the comprehension of gastric adenocarcinoma. A focus was made on the different actors of gastric carcinogenesis, including, Helicobacter pylori cancer stem cells, tumour microenvironment and microbiota. New and recent potential biomarkers were assessed as well as emerging therapeutical strategies involving cancer stem cells targeting as well as immunotherapy. Finally, recent experimental models to study this highly complex disease were discussed, highlighting the importance of gastric cancer understanding in the hard-fought struggle against cancer relapse, metastasis and bad prognosis.

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How doesHelicobacter pyloricause gastric cancer through connexins: An opinion review

Cited by 13 publications

References 180 publications

Helicobacter pylori y cáncer gástrico

Helicobacter pylori y cáncer gástrico

Helicobacter pylori in gastric cancer: Features of infection and their correlations with long-term results of treatment

Gastric Cancer: Advances in Carcinogenesis Research and New Therapeutic Strategies

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