Meta-analysis of mucosal microbiota reveals universal microbial signatures and dysbiosis in gastric carcinogenesis

Liu, Changan; Ng, Siu-Kin; Ding, Yanqiang; Lin, Yufeng; Liu, Weixin; Wong, Sunny H.; Sung, Joseph J.Y.; Yu, Jun

doi:10.1038/s41388-022-02377-9

Cited by 41 publications

(56 citation statements)

References 46 publications

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“…Furthermore, based on the current findings, a panel of differential gastric bacteria can be developed to distinguish GC and the progression of GC with outstanding performance. A recently published meta-analysis, which enrolled six independent studies, reported that eight bacterial taxa could serve as a panel of biomarkers to discriminate GC from superficial gastritis with an area under the curve (AUC) of 0.850 (Liu et al, 2022). Regarding the progression of GC, Kadeerhan et al reported a combination of four genera (Bacillus, Capnocytophaga, Helicobater, Prevotella) with age and sex to distinguish subjects after lesion progression from non-progression controls (AUC = 0.927) (Kadeerhan et al, 2021).…”

Section: The Non-h Pylori Microbes Associated With Gcmentioning

confidence: 99%

Gastric microbiota in gastric cancer: Different roles of Helicobacter pylori and other microbes

Guo

Cao

Zhou

et al. 2023

Front. Cell. Infect. Microbiol.

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Gastric cancer (GC) is one of the leading causes of cancer-related deaths worldwide. The gastric microbiota plays a critical role in the development of GC. First, Helicobacter pylori (H. pylori) infection is considered a major risk factor for GC. However, recent studies based on microbiota sequencing technology have found that non-H. pylori microbes also exert effects on gastric carcinogenesis. Following the infection of H. pylori, gastric microbiota dysbiosis could be observed; the stomach is dominated by H. pylori and the abundances of non-H. pylori microbes reduce substantially. Additionally, decreased microbial diversity, alterations in the microbial community structure, negative interactions between H. pylori and other microbes, etc. occur, as well. With the progression of gastric lesions, the number of H. pylori decreases and the number of non-H. pylori microbes increases correspondingly. Notably, H. pylori and non-H. pylori microbes show different roles in different stages of gastric carcinogenesis. In the present mini-review, we provide an overview of the recent findings regarding the role of the gastric microbiota, including the H. pylori and non-H. pylori microbes, in the development of GC.

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Section: The Non-h Pylori Microbes Associated With Gcmentioning

confidence: 99%

Gastric microbiota in gastric cancer: Different roles of Helicobacter pylori and other microbes

Guo

Cao

Zhou

et al. 2023

Front. Cell. Infect. Microbiol.

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“…The predominant role of H. pylori in GC development has triggered an increasing interest in the study of gastric dysbiosis in last decade (17). In fact, gastric microbiota composition is highly variable between individuals (18).…”

Section: Gastric Dysbiosis As a Main Player In Early Gastric Carcinog...mentioning

confidence: 99%

Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging

et al. 2023

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Upper gastrointestinal endoscopy is considered the gold standard for gastric lesions detection and surveillance, but it is still associated with a non-negligible rate of missing conditions. In the Era of Personalized Medicine, biomarkers could be the key to overcome missed lesions or to better predict recurrence, pushing the frontier of endoscopy to functional endoscopy. In the last decade, microbiota in gastric cancer has been extensively explored, with gastric carcinogenesis being associated with progressive dysbiosis. Helicobacter pylori infection has been considered the main causative agent of gastritis due to its interference in disrupting the acidic environment of the stomach through inflammatory mediators. Thus, does inflammation bridge the gap between gastric dysbiosis and the gastric carcinogenesis cascade and could the microbiota-inflammation axis-derived biomarkers be the answer to the unmet challenge of functional upper endoscopy? To address this question, in this review, the available evidence on the role of gastric dysbiosis and chronic inflammation in precancerous conditions of the stomach is summarized, particularly targeting the nuclear factor-κB (NF-κB), toll-like receptors (TLRs) and cyclooxygenase-2 (COX-2) pathways. Additionally, the potential of liquid biopsies as a non-invasive source and the clinical utility of studied biomarkers is also explored. Overall, and although most studies offer a mechanistic perspective linking a strong proinflammatory Th1 cell response associated with, but not limited to, chronic infection with Helicobacter pylori, promising data recently published highlights not only the diagnostic value of microbial biomarkers but also the potential of gastric juice as a liquid biopsy pushing forward the concept of functional endoscopy and personalized care in gastric cancer early diagnosis and surveillance.

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“…, Veillonella and Parvimonas ) was observed concomitantly with a decrease in putative probiotics ( e.g. , Bifidobacterium ) throughout the stages of disease progression[ 41 ]. Another study has suggested that successful eradication of H. pylori could reverse the tendency towards gastric microbiota dysbiosis and show beneficial effects on the gastric microbiota[ 42 ].…”

Section: Pathogenesis Of H Pylori Gastric Infectionmentioning

confidence: 99%

Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis

Melo¹,

Marques²,

Pinheiro³

et al. 2022

World J Clin Oncol

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Gastric cancer is the fifth most common malignancy and third leading cancer-related cause of death worldwide. Helicobacter pylori is a Gram-negative bacterium that inhabits the gastric environment of 60.3% of the world’s population and represents the main risk factor for the onset of gastric neoplasms. CagA is the most important virulence factor in H. pylori , and is a translocated oncoprotein that induces morphofunctional modifications in gastric epithelial cells and a chronic inflammatory response that increases the risk of developing precancerous lesions. Upon translocation and tyrosine phosphorylation, CagA moves to the cell membrane and acts as a pathological scaffold protein that simultaneously interacts with multiple intracellular signaling pathways, thereby disrupting cell proliferation, differentiation and apoptosis. All these alterations in cell biology increase the risk of damaged cells acquiring pro-oncogenic genetic changes. In this sense, once gastric cancer sets in, its perpetuation is independent of the presence of the oncoprotein, characterizing a “hit-and-run” carcinogenic mechanism. Therefore, this review aims to describe H. pylori - and CagA-related oncogenic mechanisms, to update readers and discuss the novelties and perspectives in this field.

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Meta-analysis of mucosal microbiota reveals universal microbial signatures and dysbiosis in gastric carcinogenesis

Cited by 41 publications

References 46 publications

Gastric microbiota in gastric cancer: Different roles of Helicobacter pylori and other microbes

Gastric microbiota in gastric cancer: Different roles of Helicobacter pylori and other microbes

Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging

Influence of Helicobacter pylori oncoprotein CagA in gastric cancer: A critical-reflective analysis

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