Helicobacter pyloriInduces Increased Expression of Toll-Like Receptors and Decreased Toll-Interacting Protein in Gastric Mucosa that Persists Throughout Gastric Carcinogenesis

Helicobacter ◽  
2012 ◽  
Vol 18 (1) ◽  
pp. 22-32 ◽  
Author(s):  
Pedro Pimentel-Nunes ◽  
Nádia Gonçalves ◽  
Inês Boal-Carvalho ◽  
Luís Afonso ◽  
Paula Lopes ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Gastric Carcinogenesis ◽  
Toll Like Receptors ◽  
Interacting Protein

scholarly journals Effect of Helicobacter pylori Eradication on Epigenetic Changes in Gastric Cancer-related Genes

2021 ◽  
Vol 21 (4) ◽  
pp. 256-266
Author(s):  
Ji Min Choi ◽  
Sang Gyun Kim
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Gastric Carcinogenesis ◽  
Point Of View ◽  
Epigenetic Changes ◽  
Epigenetic Alterations ◽  
Helicobacter Pylori Eradication ◽  
Gastric Cancer Prevention ◽  
H Pylori

It is known that gastric carcinogenesis results from the progressive changes from chronic gastritis to gastric atrophy, intestinal metaplasia, dysplasia, and invasive carcinoma. Several genetic and epigenetic alterations are involved in this process, and Helicobacter pylori (H. pylori) infection is believed to induce the initiation and progression of these steps. From an epigenetic point of view, H. pylori induces hypermethylation of genes involved in the development of gastric cancer and regulates the expression of various microRNAs (miRNAs). These H. pylori-related epigenetic changes are accumulated not only at the site of neoplasm but also in the adjacent non-cancerous gastric mucosa. Thereby, a state vulnerable to gastric cancer known as an epigenetic field defect is formed. H. pylori eradication can have an effective chemopreventive effect in gastric carcinogenesis. However, the molecular biological changes that occur in the stomach environment during H. pylori eradication have not yet been established. Several studies have reported that H. pylori eradication can restore infection-related changes, especially epigenetic alterations in gastric cancer-related genes, but some studies have shown otherwise. Simply put, it appears that the recovery of methylated gastric cancer-related genes and miRNAs during H. pylori eradication may vary among genes and may also differ depending on the histological subtype of the gastric mucosa. In this review, we will discuss the potential mechanism of gastric cancer prevention by H. pylori eradication, mainly from an epigenetic perspective.

Differential expression of human telomerase reverse transcriptase β-site remaining alternative splicing variants (hTERT β+ ASV) in gastric carcinogenesis

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e15641-e15641
Author(s):  
X. Geng
Keyword(s):  
Gastric Cancer ◽  
Enzyme Activity ◽  
Alternative Splicing ◽  
Gastric Mucosa ◽  
Precancerous Lesions ◽  
Normal Mucosa ◽  
Gastric Carcinogenesis ◽  
Normal Gastric Mucosa ◽  
Rt Pcr ◽  
Splicing Variants

e15641 Background: To investigate the changes of hTERT alternative splicing variants pattern in gastric cancer, precancerous lesions and normal gastric mucosa tissue. Methods: Three alternative splicing sites (α, β, γ) were selected and designed PCR primer. The expression of 8 hTERT alternative splicing variants (ASVs) in gastric cancer, precancerous lesions and normal gastric mucosa were detected by Semi-nested RT-PCR. The expression of β-site remaining ASV (β+ASV) in specimens of gastric cancer and specimens of precancerous lesions was detected by SYBER Green real-time PCR. Telomerase enzyme activity was evaluated associated with the different hTERT ASVs. Results: The positive rate of active full-length (α+β+γ+ ) ASV was significantly higher in gastric cancer than in precancerous lesions and normal mucosa (94.7% vs. 40.0% and 0, P<0.05). The positive rates of other ASVs were not different among the 3 groups(P>0.05). The positive rates of β+ ASVs (including α+β+γ+ASV, α-deletion ASV, γ-deletion ASV, αγ-deletion ASV) were 11.1% in normal mucosa,40.0% in precancerous lesions and 94.7% in gastric cancer (P<0.05). SYBR Green real-time RT-PCR showed that the expression level of β+ASV was 6.99 times higher in gastric cancer than in precancerous lesions. Further, increased telomerase enzyme activity was only associated with expression of the full-length hTERT isoform. Conclusions: hTERT alternative splicing pattern is different during gastric carcinogenesis. β+ASV was widely expressed in gastric carcinogenesis and may provide some information for diagnosis of gastric cancer or precancerous lesions. The gene expression patterns of hTERT alternative splicing variants may provide some useful information for diagnosis of gastric cancer and precancerous lesions. No significant financial relationships to disclose.

scholarly journals Toll-Like Receptors as Biomarkers of Gastric Carcinogenesis: Implications for Diagnosis, Prognosis and Treatment

2013 ◽  
Vol 04 (05) ◽  
pp. 1037-1047
Author(s):  
Pedro Pimentel-Nunes ◽  
João Bruno Soares ◽  
Mário Dinis-Ribeiro
Keyword(s):  
Gastric Carcinogenesis ◽  
Toll Like Receptors
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