Relevance of <i>Helicobacter pylori vac</i>A 3ʹ‐end Region Polymorphism to Gastric Cancer

Bakhti, Seyedeh Zahra; Latifi‐Navid, Saeid; Mohammadi, Shiva; Zahri, Saber; Bakhti, Fatemeh Sadat; Feizi, Farideh; Yazdanbod, Abbas; Siavoshi, Farideh

doi:10.1111/hel.12284

Cited by 40 publications

(35 citation statements)

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“…The same failure was found for value of differences in the 3′ end region of vacA , denoted by c1 and c2 (c1 thought to be more harmful than the c2), which were reported to be strong predictors for gastric cancer in men (Ref. 74). The failure of predictions to achieve consistency across populations most likely reflects different evolution of vacA in different populations such that the association is primary with the population with disease associations occurring by chance.…”

Section: Search For a Cancer-specific H Pylori Gene Or Virulence Factorsupporting

confidence: 59%

Helicobacter pylorias an oncogenic pathogen, revisited

Miftahussurur¹,

Yamaoka²,

Graham³

2017

Expert Rev. Mol. Med.

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Gastric cancer is an inflammation-associated malignancy aetiologically related to infection with the bacterium, Helicobacter pylori, which is considered a necessary but insufficient cause. Unless treated, H. pylori causes life-long acute and chronic gastric inflammation resulting in progressive gastric mucosal damage that may result in gastric cancer. The rate of progression from superficial gastritis, to an atrophic metaplastic mucosa, and ultimately to cancer relates to the virulence of the infecting H. pylori as well as host and environmental factors. H. pylori virulence is a reflection of its propensity to cause severe gastric inflammation. Both mucosal inflammation and H. pylori can cause host genomic instability, including dysregulation of DNA mismatch repair, stimulation of expression of activation-induced cytidine deaminase, abnormal DNA methylation and dysregulation of micro RNAs, which may result in an accumulation of mutations and loss of normal regulation of cell growth. The difference in cancer risk between the most and least virulent H. pylori strain is only approximately 2-fold. Overall, none of the putative virulence factors identified to date have proved to be disease-specific. The presence, severity, extent and duration of inflammation appear to be the most important factors and current evidence suggests that any host, environmental or bacterial factor that reliably enhances the inflammatory response to the H. pylori infection increases the risk of gastric cancer.

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Section: Search For a Cancer-specific H Pylori Gene Or Virulence Factorsupporting

confidence: 59%

Helicobacter pylorias an oncogenic pathogen, revisited

Miftahussurur¹,

Yamaoka²,

Graham³

2017

Expert Rev. Mol. Med.

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“…Gastric cancer is one of the most common diseases related to H. pylori infection, responsible for approximately 75% of gastric cancer incidents worldwide [26][27][28][29]. The discrepancy in the severity of gastric cancer is associated with many factors and mechanisms, among which various genotypes of H. pylori strains play a role [30][31][32][33][34][35][36][37][38][39][40]. H. pylori induces other diseases of the alimentary tract, including gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue lymphoma, GERD symptoms, and dyspepsia [41][42][43][44][45][46].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world's population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

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“…e VacA is a poreforming toxin, which causes progressive vacuolation and injury to the gastric epithelium [25]. It is associated with an increased risk of PUD and GC [26,27]. Specific allelic types in the vacA gene are signal (s1, s2) and the middle regions (m1, m2) due to sequence heterogeneity [28].…”

Section: Introductionmentioning

confidence: 99%

Precancerous Gastric Lesions with Helicobacter pylori vacA⁺/babA2⁺/oipA⁺ Genotype Increase the Risk of Gastric Cancer

Bartpho

Wattanawongdon

Tongtawee

et al. 2020

BioMed Research International

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Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.

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Relevance of Helicobacter pylori vacA 3ʹ‐end Region Polymorphism to Gastric Cancer

Abstract: The H. pylori vacA c1 genotype might therefore be one of the strongest risk predictors of GC in male patients aged ≥55 in Iran.

Cited by 40 publications

References 42 publications

Helicobacter pylorias an oncogenic pathogen, revisited

Helicobacter pylorias an oncogenic pathogen, revisited

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Precancerous Gastric Lesions with Helicobacter pylori vacA⁺/babA2⁺/oipA⁺ Genotype Increase the Risk of Gastric Cancer

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Relevance of Helicobacter pylori vacA 3ʹ‐end Region Polymorphism to Gastric Cancer

Abstract: The H. pylori vacA c1 genotype might therefore be one of the strongest risk predictors of GC in male patients aged ≥55 in Iran.

Cited by 40 publications

References 42 publications

Helicobacter pylorias an oncogenic pathogen, revisited

Helicobacter pylorias an oncogenic pathogen, revisited

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer

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Product

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Precancerous Gastric Lesions with Helicobacter pylori vacA⁺/babA2⁺/oipA⁺ Genotype Increase the Risk of Gastric Cancer