Lectin histochemistry of galactose andN-acetyl-galactosamine glycoconjugates in normal gastric mucosa and gastric cancer and the relationship with ABO and secretor status

1986 ◽  
Vol 150 (2) ◽  
pp. 135-144 ◽  
Author(s):  
J. C. Macartney
2017 ◽  
Vol 14 (3) ◽  
pp. 3705-3710 ◽  
Author(s):  
Bide Liu ◽  
Yu Zhou ◽  
Dan Lu ◽  
Yong Liu ◽  
Si-Quan Zhang ◽  
...  

2011 ◽  
Vol 49 (1) ◽  
pp. 142-147 ◽  
Author(s):  
Mariusz Gryko ◽  
Katarzyna Guzińska-Ustymowicz ◽  
Anna Pryczynicz ◽  
Dariusz Cepowicz ◽  
Adam Kukliński ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Fasciana Teresa ◽  
Nicola Serra ◽  
Giuseppina Capra ◽  
Chiara Mascarella ◽  
Cesare Gagliardi ◽  
...  

Introduction. Helicobacter pylori and Epstein–Barr virus (EBV) infection have recently been shown to be associated with gastric diseases. Polymorphisms in genes encoding cytokines such as interleukin 10 (IL-10) and interleukin 1 Receptor (IL-1RN) influence cytokine secretion levels and appear to contribute to the risk of developing gastroduodenal diseases. To our knowledge, this is the first preliminary study to address the association of coinfection with H. pylori and EBV and their correlation with genetic predisposition in the development of gastric diseases. Methods. Gastric biopsy samples of 96 patients with different gastric diseases were used. Results. Our results showed that the rate of coinfection was higher in patients with gastric cancer than in patients with normal gastric mucosa, active chronic gastritis, and MALT lymphoma. As regards the characterization of H. pilory strains, the polymorphism s1m1i1 of vacA gene was more frequent in patients with MALT Lymphoma in comparison to others, while the polymorphism s2m2i2 was most frequent in patients with normal gastric mucosa. In addition, patients who tested positive for the cagA gene were more frequently those affected with gastric cancer than those with inactive chronic gastritis. Similarly, the patients with oipA gene ON were more frequently those with gastric cancer than those with inactive chronic gastritis. Conclusion. According to our analysis, there was no correlation between coinfection and polymorphisms in genes encoding IL-10 and IL-1RN. We conclude that various factors can be involved in the development of gastric diseases.


2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e15641-e15641
Author(s):  
X. Geng

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.


Author(s):  
A. O. Sablina ◽  
O. A. Sablin ◽  
S. S. Aleksanin ◽  
G. G. Rodionov ◽  
I. I. Shantyr' ◽  
...  

Relevance. Today gastric cancer is still one of the oncologic diseases most often leading to death. H. pylori eradication reduces risk of gastric cancer, but its efficacy depends on gastric mucosa state. Atrophy of gastric mucosa is more common in Chernobyl nuclear power plant (CNPP) accident recovery workers than in patients who have not been involved in CNPP accident recovery works. It seems especially important to investigate the features of antibiotics transport to H. pylori colonization area in this contingent.Intention – to determine the features of amoxicillin secretion by gastric mucosa in CNPP accident recovery workers with atrophic and nonatrophic gastritis undergoing H. pylori eradication.Methodology. 65 CNPP accident recovery workers were divided into groups depending on state of gastric mucosa according to endoscopic and histological examination, immunosorbent assay of pepsinogens I and II and gastrin-17 basal serum levels. On the first day of eradication therapy, gastric secretion samples were obtained via nasogastric probe 30, 60, 120, 180 and 240 minutes after oral amoxicillin administration. Drug concentrations in gastric secretion were assessed via liquid chromatography-mass spectrometry.Results and discussion. Amoxicillin concentrations in gastric secretion samples were lower (р < 0.01) in patients with atrophic antral gastritis than in patients with normal gastric mucosa and atrophic fundal gastritis. Patients with fundal atrophy were characterized by lower amoxicillin concentrations 30 and 60 (p = 0.02) minutes after drug intake than in patients with normal gastric mucosa, and higher concentration in the 120th (p < 0.01) and 180th (p = 0.02) minute than in patients with antral atrophy. Amoxicillin concentrations in patients with antral atrophy were lower (p < 0.01) than in non-atrophy group in the 30th, 60th and 120th minute. In the 240th minute, amoxicillin concentrations in patients with fundal atrophy exceeded concentrations in both other groups (p < 0.01). Amoxicillin concentration peak was registered in patients with fundal and antral atrophy in the 180th minute, in patients without atrophy – from the 30th to 120th minute.Conclusion. Atrophy of gastric mucosa is characterized by decreased transport of orally administered amoxicillin from bloodstream to gastric lumen. Depending on gastric mucosa state, amoxicillin concentrations in gastric secretion should be evaluated at different time points after drug administration: in patients with atrophic gastritis – in the 180th minute, in patients without atrophy – in the 120th minute. While predicting the efficacy and choosing H. pylori eradication regimen, morphological and functional state of gastric mucosa should be taken into account.


2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Sifeng Hu ◽  
Fanmei Meng ◽  
Xiankun Yin ◽  
Changling Cao ◽  
Guangyong Zhang

AbstractEcto-5′-nucleotidase (NT5E) is a glycosylphosphatidylinositol anchored cell surface protein, and has been suggested to be dysregulated in most types of human cancer including gastric cancer. The aim of the present study was to present more evidence about the clinical and prognostic value of Ecto-5′-nucleotidase in gastric cancer patients, and preliminarily explore the biological function of Ecto-5′-nucleotidase in gastric cancer cells. In our study, high Ecto-5′-nucleotidase expression was observed in gastric cancer tissues and cell lines, respectively, compared with normal gastric mucosa tissues cells. Meanwhile, TCGA database also indicated that Ecto-5′-nucleotidase expression levels were notably elevated in gastric cancer tissues compared with normal gastric mucosa tissues. Furthermore, high-expression of Ecto-5′-nucleotidase was obviously associated with advanced clinical stage, deep tumor invasion, lymph node metastasis and distant metastasis in gastric cancer patients. The survival analyses of TCGA database and our study consistent suggested high Ecto-5′-nucleotidase expression was negatively correlated with overall survival time in gastric cancer patients. The univariate and multivariate Cox proportional hazards regression model showed high Ecto-5′-nucleotidase expression was an independent poor prognostic factor for gastric cancer patients. Moreover, silencing of Ecto-5′-nucleotidase expression suppressed cell proliferation, migration and invasion in vitro in gastric cancer. In conclusion, Ecto-5′-nucleotidase is a credible prognostic biomarker, and serves as a potential therapeutic target in gastric cancer.


2021 ◽  
Author(s):  
Yuka Hirashita ◽  
Masahide Fukuda ◽  
Masaaki Kodama ◽  
Yoshiyuki Tsukamoto ◽  
Tadayoshi Okimoto ◽  
...  

Abstract Background Although eradication therapy for chronic Helicobacter pylori reduces the risk of gastric cancer (GC), its effectiveness is incomplete. Therefore, it is critically important to identify those patients who remain at high risk after H. pylori eradication therapy. Accumulation of protein methylation is strongly implicated in cancer, and a recent study showed that dimethylation of eEF1A lysine 55 (eEF1AK55me2) promotes carcinogenesis in vivo. We aimed to investigate the relationship between eEF1A dimethylation and H. pylori status in gastric mucosa and to reveal potential downstream molecules of eEF1A dimethylation in H. pylori-eradicated mucosa. Methods Records of 115 patients (11 H. pylori-negative, 29 H. pylori-positive, 75 post-eradication patients) who underwent upper gastrointestinal endoscopy were retrospectively reviewed. The eEF1A dimethyl level was evaluated in each functional cell type of gastric mucosa by immunofluorescent staining. We also investigated the relationship between eEF1AK55me2 downregulation by CRISPR/Cas9-mediated deletion of Mettl13, which is known as a dimethyltransferase of eEF1AK55me2. Results The level of eEF1A dimethylation significantly increased in the surface and basal areas of H. pylori-positive mucosa compared with -negative mucosa (surface, p=0.0031; basal, p<0.0001). The eEF1A dimethyl levels in the surface area were significantly reduced by eradication therapy (p=0.005), but those in the basal area were maintained even after eradication therapy. Multivariate analysis revealed that high dimethylation of eEF1A in the basal area of the mucosa was the independent factor related to GC incidence (odds ratio=3.6611, 95% confidence interval=1.0350–12.949, p=0.0441). We also showed the relationship between eEF1A dimethylation and expressions of reprogramming factors Oct4 and Nanog by immunohistochemistry and in vitro genome editing experiments. Conclusions The results indicated that H. pylori infection potently induced eEF1A dimethylation in gastric mucosa. The accumulation of dimethyl-eEF1A in the basal area of the mucosa might contribute to GC risk via regulation of reprograming factors in H. pylori-eradicated gastric mucosa.


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