Oxidative DNA Damage as a Potential Early Biomarker of Helicobacter pylori Associated Carcinogenesis

  title={Oxidative DNA Damage as a Potential Early Biomarker of Helicobacter pylori Associated Carcinogenesis},
  author={Yasir Raza and Adnan Khan and Amber Farooqui and Muhammad Mubarak and Alexander Facista and Syed Shakeel Akhtar and Saeed M. Khan and Javed Iqbal Kazi and Carol Bernstein and Shahana Urooj Kazmi},
  journal={Pathology \& Oncology Research},
Helicobacter pylori infection is an established risk factor for gastritis, gastric ulcer, peptic ulcer and gastric cancer. CagA +ve H. pylori has been associated with oxidative DNA damage of gastric mucosa but their combined role in the development of gastric cancer is still unknown. Here we compare the combined expression of cagA and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in normal, gastritis and gastric cancer tissues. Two hundred gastric biopsies from patients with dyspeptic symptoms, 70… 

Serum 8 Hydroxydeoxyguanosine and Cytotoxin Associated Gene A as Markers for Helicobacter pylori Infection.

Individual infected with H.pylori bearing CagA strains have the highest serum 8OHdG level and eradication therapy decreases the serum 8 OHdGlevel, which may be a good marker for prevention from gastric adenocarcinoma.

Helicobacter pylori and Its Virulence Factors' Effect on Serum Oxidative DNA Damages in Adults With Dyspepsia.

The presence of cagA and babA virulence factors may be associated with increased serum 8-OHdG in dyspeptic patients and may induce the damage to gastric cells.

Crosstalk Between DNA Damage and Inflammation in the Multiple Steps of Gastric Carcinogenesis.

Mechanisms, by which the bacteria-induced inflammation in gastric mucosa leads to intestinal metaplasia and carcinoma, are represented in this review.

Impact of Helicobacter pylori Infection and Its Major Virulence Factor CagA on DNA Damage Repair

The role of CagA is accentuated as a significant contributor of H. pylori infection-mediated DDR modulation, potentially disrupting the balance between DNA damage and repair, thus favoring genomic instability and carcinogenesis.

Helicobacter pylori induces somatic mutations in TP53 via overexpression of CHAC1 in infected gastric epithelial cells

Findings indicate that H. pylori‐mediated CHAC1 overexpression degrades intracellular glutathione, allowing the accumulation of ROS which subsequently causes mutations that could contribute to the development of gastric cancer.

Helicobacter pylori‐induced DNA double‐stranded break in the development of gastric cancer

Infection with cagA‐positive Helicobacter pylori strains plays an etiological role in the development of gastric cancer and CagA–SHP2 interaction aberrantly activates SHP2 and thereby deregulates Ras–ERK signaling.

Evaluation of mutagenesis, necrosis and apoptosis induced by omeprazole in stomach cells of patients with gastritis

The continuous and prolonged omeprazole use induces genetic instability, which can be monitored through cytogenetic analyzes, as precursor for gastric cancer.

Helicobacter pylori Thioredoxin1 May Play a Highly Pathogenic Role via the IL6/STAT3 Pathway

HP Trx1 may play as a marker of high pathogenicity, and the high-Trx1 HP could mediate the pathogenic process of HP infection via the IL6/STAT3 pathway.

Role of Bacterial and Viral Pathogens in Gastric Carcinogenesis

This review updates on recent discoveries, focusing on the roles of various gastric pathogens and gastric microbiome in tumorigenesis, and discusses how Gastric pathogens induce tumorigenic changes in the stomach.



Role of Helicobacter pylori CagA + Infection in Determining Oxidative DNA Damage in Gastric Mucosa

A significant correlation was found between ROS production and 8-OHdG content, which could support the hypothesis that the oxygen-free radicalsmediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.

Influence of Helicobacter pylori on reactive oxygen-induced gastric epithelial cell injury.

Alteration in the activity of ROS-scavenging enzymes by the presence of H. pylori may in part be responsible for the increased risk of gastric cancer in persons infected with H.pylori.

Helicobacter pylori CagA-positive strains affect oxygen free radicals generation by gastric mucosa.

Gastric mucosa of patients infected byHP-CagA-positive strains is characterized by a higher generation of ROMs and by greater neutrophil counts than that observed in HP-CAGA-negative subjects, which might be relevant in the pathogenesis of gastric malignancies.

Helicobacter pylori, inflammation, oxidative damage and gastric cancer: a morphological, biological and molecular pathway

  • F. FarinatiR. Cardin M. Rugge
  • Medicine, Biology
    European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation
  • 2008
It is best to monitor patients harboring NiN closely with endoscopy and extensive bioptic sampling, and to eradicate any H. pylori to prevent the accumulation of oxidative DNA damage and its consequent progression, as the growing body of evidence of the regression of precancerous changes and the high prevalence of superficial gastric carcinoma demonstrated in long-term follow-up studies on NiN make this approach mandatory.

Detection of Helicobacter pylori in gastric biopsy and resection specimens.

Investigation of the sensitivity of detecting Helicobacter pylori in gastric biopsy and resection specimens using tinctorial and silver impregnation stains, immunohistochemistry and the polymerase chain reaction found it to be highly sensitive and easy to use.

Helicobacter pylori infection in gastric cancerogenesis.

This overview attempts to summarize the recent basic and clinical evidence on the link between H. pylori and gastric cancer, after the award of the Nobel Prize for Physiology or Medicine to Drs.

Helicobacter pylori infection and gastric cancer risk: evaluation of 15 H. pylori proteins determined by novel multiplex serology.

GroEL was identified as a new independent risk marker that may contribute to enhanced quantification of H. pylori-related GC risk and CagA and GroEL were found to be independent predictors of GC.

Helicobacter pylori and gastric carcinogenesis

The oncogenic potential of CagA may be further potentiated in the presence of chronic inflammation, which aberrantly induces activation-induced cytidine deaminase (AID), a member of the DNA/RNA-editing enzyme family.

Helicobacter pylori cagA and vacA Genotypes as Predictors of Progression of Gastric Preneoplastic Lesions: A Long-Term Follow-Up in a High-Risk Area in Spain

H. pylori genotyping may be useful for the identification of patients at high risk of progression of gastric preneoplastic lesions and who need more intensive surveillance.

Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk

The host immune response is discussed and other host factors that increase the pathogenic potential of this bacterium are examined, including host polymorphisms, alterations to the apical-junctional complex, and the effects of environmental factors.