Helicobacter pylori and gastric cancer

Pritchard, D. Mark; Je, Crabtree

doi:10.1097/01.mog.0000245539.50765.f6

Cited by 41 publications

(34 citation statements)

References 72 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At the later time points of the study (6,9, and 12 mo postinfection), bacterial colonization decreased progressively in the majority of mice (Fig. 1A).…”

Section: Chronic Infection Of C57bl/6 Mice With H Felis Results In Gmentioning

confidence: 99%

“…Whereas ϳ20% of infected individuals develop symptomatic disease, the large majority remains asymptomatic despite persistent, often lifelong colonization with the bacterium. This wide diversity in colonization outcome has been attributed to strain differences (Western vs Eastern Helicobacter strains), genetically determined host susceptibility, and lifestyle factors such as nutrition and hygiene (6). However, no single universal explanation has yet been found to hold true across all populations studied, and it is likely that a combination of multiple factors determines infection outcome.…”

mentioning

confidence: 99%

See 1 more Smart Citation

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

Sayi

Kohler

Hitzler

et al. 2009

The Journal of Immunology

152

184

View full text Add to dashboard Cite

show abstract

“…At the later time points of the study (6,9, and 12 mo postinfection), bacterial colonization decreased progressively in the majority of mice (Fig. 1A).…”

Section: Chronic Infection Of C57bl/6 Mice With H Felis Results In Gmentioning

confidence: 99%

mentioning

confidence: 99%

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

Sayi

Kohler

Hitzler

et al. 2009

The Journal of Immunology

152

184

View full text Add to dashboard Cite

show abstract

“…Recently, the direct interaction between this bacterial pathogen and fibroblasts has been proposed16 suggesting that H. pylori can interact with several components of connective tissue components including fibroblasts. The most virulent H. pylori strains have been shown to harbor the cag pathogenicity island encoding the type IV secretion system,3, 17 allowing the delivery of bacterial cytotoxins into gastric epithelial cells, inducing phenotypic alterations reminiscent of an epithelial to mesenchymal transition (EMT) 3, 17, 18, 19…”

Section: Introductionmentioning

confidence: 99%

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

et al. 2018

View full text Add to dashboard Cite

BackgroundMajor human gastrointestinal pathogen Helicobacter pylori (H. pylori) colonizes the gastric mucosa causing inflammation and severe complications including cancer, but the involvement of fibroblasts in the pathogenesis of these disorders in H. pylori‐infected stomach has been little studied. Normal stroma contains few fibroblasts, especially myofibroblasts. Their number rapidly increases in the reactive stroma surrounding inflammatory region and neoplastic tissue; however, the interaction between H. pylori and fibroblasts remains unknown. We determined the effect of coincubation of normal rat gastric fibroblasts with alive H. pylori (cagA+vacA+) and H. pylori (cagA−vacA−) strains on the differentiation of these fibroblasts into cells possessing characteristics of cancer‐associated fibroblasts (CAFs) able to induce epithelial‐mesenchymal transition (EMT) of normal rat gastric epithelial cells (RGM‐1).Materials and MethodsThe panel of CAFs markers mRNA was analyzed in H. pylori (cagA+vacA+)‐infected fibroblasts by RT‐PCR. After insert coculture of differentiated fibroblasts with RGM‐1 cells from 24 up to 48, 72, and 96 hours, the mRNA expression for EMT‐associated genes was analyzed by RT‐PCR.ResultsThe mRNA expression for CAFs markers was significantly increased after 72 hours of infection with H. pylori (cagA+vacA+) but not H. pylori (cagA−vacA−) strain. Following coculture with CAFs, RGM‐1 cells showed significant decrease in E‐cadherin mRNA, and the parallel increase in the expression of Twist and Snail transcription factors mRNA was observed along with the overexpression of mRNAs for TGFβR, HGFR, FGFR, N‐cadherin, vimentin, α‐SMA, VEGF, and integrin‐β1.Conclusion Helicobacter pylori (cagA+vacA+) strain induces differentiation of normal fibroblasts into CAFs, likely to initiate the EMT process in RGM‐1 epithelial cell line.

show abstract

“…adenovirus) (Evans et al, 2007;Nava et al, 2004;Walters et al, 2002). Another striking example is provided by the bacterium Helicobacter pylori, which causes gastric ulcers and cancer (Pritchard and Crabtree, 2006). H. pylori translocates a protein called CagA into host cells.…”

Section: Tjs In Diseasementioning

confidence: 99%

Tight junctions at a glance

Balda

Matter

2008

Journal of Cell Science

212

168

View full text Add to dashboard Cite

Helicobacter pylori and gastric cancer

Abstract: Complex interactions between several bacterial, host genetic and environmental factors determine whether H. pylori infected individuals develop gastric carcinoma. The importance of bone marrow stem cell engraftment during human gastric neoplasia is an area requiring urgent investigation.

Cited by 41 publications

References 72 publications

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

Tight junctions at a glance

Contact Info

Product

Resources

About