Is There a Role for the Non-Helicobacter pylori Bacteria in the Risk of Developing Gastric Cancer?

Li, Jackie; Perez, Guillermo I. Perez

doi:10.3390/ijms19051353

Cited by 32 publications

(33 citation statements)

References 51 publications

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“…Previous researchers defined a positive H pylori infection as having an RA ≥ 2% . Therefore, we categorized H pylori infection status as follows: Helicobacter RA ≥ 2% was considered positive and RA < 2% was considered negative.…”

Section: Resultsmentioning

confidence: 99%

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Gastric mucosal microbiota in a Mongolian population with gastric cancer and precursor conditions

Gantuya

Serag

Matsumoto

et al. 2020

Aliment Pharmacol Ther

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Summary Background Incidence and mortality of gastric cancer (GC) are high in Mongolia despite Helicobacter pylori in the Mongolian population being less virulent. Aim To evaluate gastric bacterial microbiota profiles in patients with GC and its precursor histological conditions. Methods We conducted a case‐control study among 48 GC and 120 noncancer patients (20 normal gastric mucosa [control], 20 gastritis, 40 with atrophy and 40 intestinal metaplasia [IM]). We performed 16S rRNA gene amplicon sequencing and compared taxonomic and functional prediction profiles based on the diagnosis group and H pylori infection status. Results The highest overall bacterial alpha diversity metrics were observed in the control group, followed by the IM and cancer groups. The gastritis and atrophy groups had the least diversity. Lactobacilli and Enterococci were the dominant genus in several cancer patients especially in the absence of H pylori. In addition, Carnobacterium, Glutamicibacter, Paeniglutamicibacter, Fusobacterium and Parvimonas were associated with GC regardless of H pylori infection. Firmicutes were decreased in the gastritis and atrophy groups and increased in the IM and cancer groups. The functional metabolic activity of the Embden‐Meyerhof‐Parnas pathway and the utilization of sugar, were significantly increased in cancer group compared with the noncancer group. Conclusion Microbial factors other than H pylori may play a role in Mongolian GC. We identified novel associations between GC and the genera Enterococcus, Lactobacillus, Carnobacterium, Glutamicibacter, Paeniglutamicibacter, Fusobacterium, and Parvimonas.

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Section: Resultsmentioning

confidence: 99%

“…Previous researchers defined a positive H pylori infection as having an RA ≥ 2%. 18 (Figure 2A) or excluding cases with dominant bacterial genera or Helicobacter-positive status ( Figure 2B).…”

Section: Multivariate Taxonomic Analysis Of Gc and Its Precursor DImentioning

confidence: 99%

Gastric mucosal microbiota in a Mongolian population with gastric cancer and precursor conditions

Gantuya

Serag

Matsumoto

et al. 2020

Aliment Pharmacol Ther

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“…Infection with H. pylori , which is characterized as highly pathogenic and difficult to eradicate, is the major cause of GC . However, the molecular mechanisms underlying H. pylori infection‐mediated GC are still largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori CagA promotes the malignant transformation of gastric mucosal epithelial cells through the dysregulation of the miR‐155/KLF4 signaling pathway

Ren

Zhao

et al. 2019

Molecular Carcinogenesis

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The Helicobacter pylori (H. pylori) cytotoxin-associated gene A (CagA) and Krüppel-like transcription factor (KLF4) were both closely associated with the development and progression of gastric cancer (GC). However, the nature of the interactions between CagA and KLF4 in GC development has not been elucidated. Therefore, we focused on the CagA-mediated promotion of the malignant transformation of gastric epithelial cells. Herein, we first examined the expression of KLF4 in both human cancer and paracarcinoma tissues with or without H. pylori infection and found that KLF4 expression was significantly decreased in H. pylori-positive GC cells compared with the H. pylori-negative GC cells. Further functional studies revealed that the increased expression of CagA could suppress KLF4 expression and promote the malignant transformation of normal epithelial cells. Subsequently, we found that CagA could upregulate miR-155 and further restrict the expression of downstream KLF4. More importantly, the overexpression of miR-155 in GES-1 promoted epithelial-mesenchymal transition and eventually facilitated tumor growth in vivo. Overall, the identification of the CagA/miR-155/KLF4 signaling pathway provided a new insight into the development and treatment of GC. K E Y W O R D S CagA, gastric cancer, Helicobacter pylori, Krüppel-like factor 4, miR-155

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“…In other words, IM transformation is just one of the "faces" of atrophy involved in the cancer-prone atrophic microenvironment. [56][57][58][59] More ambitious future efforts should focus on combining the histological and endoscopic gastritis phenotypes in an integrated staging system with a view to making cancer prediction more sensitive and specific. 49…”

Section: The S Tag Ing Fr Ame Work For G a S Tritis His Tology Rep mentioning

confidence: 99%

Gastric cancer prevention targeted on risk assessment: Gastritis OLGA staging

et al. 2019

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Gastric cancer (GC) ranks among the most lethal epithelial malignancies, and its striking mortality rate prompts a global prevention strategy. Helicobacter pylori (H. pylori) gastritis is the main GC promoter, and the 2014 Global Kyoto conference recognized H. pylori gastritis as a (treatable) infectious disease. It is therefore plausible that any large‐scale intervention for H. pylori eradication would result in cleansing the world of the fifth cause of cancer‐related death. Atrophic gastritis is the cancerization field in which GCs (both intestinal and diffuse histotypes) mainly develop. Discontinuing the inflammatory cascade triggered by H. pylori is tantamount to preventing GC. For patients (still infected or eradicated) who have already developed gastric atrophy, the severity/topography of the atrophic changes correlates with their cancer risk. Gastritis OLGA (Operative Link for Gastritis Assessment) staging consistently ranks the atrophy‐associated cancer risk, providing a solid clinical/biological rationale for establishing patient‐specific surveillance programs. By combining primary and secondary prevention strategies, gastric cancer is a preventable disease.

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Is There a Role for the Non-Helicobacter pylori Bacteria in the Risk of Developing Gastric Cancer?

Cited by 32 publications

References 51 publications

Gastric mucosal microbiota in a Mongolian population with gastric cancer and precursor conditions

Gastric mucosal microbiota in a Mongolian population with gastric cancer and precursor conditions

Helicobacter pylori CagA promotes the malignant transformation of gastric mucosal epithelial cells through the dysregulation of the miR‐155/KLF4 signaling pathway

Gastric cancer prevention targeted on risk assessment: Gastritis OLGA staging

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