The Risk of Gastric Cancer in Patients with Duodenal and Gastric Ulcer: Research Progresses and Clinical Implications

Zhang, Zun-Wu

doi:10.1007/s12029-008-9015-1

Cited by 9 publications

(9 citation statements)

References 72 publications

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“…The more diffuse model for the progression from chronic AG to intestinal metaplasia, dysplasia and finally GC takes into consideration several steps; and it considers the HP infection as acting together with a variety of host genetic and environmental factors (21). Moreover, in patients with DU, more often mild AG occurs, and there is no increased risk of GC compared with risk in the general population (22,23). At present, there is still a lack of proteomics data for markers of patient tendency to develop AAG.…”

Section: O L M E D 2 0 : 5 7 -7 1 2 0 1 4 | R E P E T T O E T a Lmentioning

confidence: 99%

Differential Proteomics of Helicobacter pylori Associated with Autoimmune Atrophic Gastritis

Repetto

Zanussi

Casarotto

et al. 2013

Mol Med

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Section: O L M E D 2 0 : 5 7 -7 1 2 0 1 4 | R E P E T T O E T a Lmentioning

confidence: 99%

Differential Proteomics of Helicobacter pylori Associated with Autoimmune Atrophic Gastritis

Repetto

Zanussi

Casarotto

et al. 2013

Mol Med

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“…Table S3 shows the classification results. Although from the clinical point of view, DU has the negtive correlation with GC among all gastroduodenal diseases [40], the classification performance of two subtype groups was only slightly improved. Thus cancer-related CagA strains might have some unique sequence patterns comparing to all other gastroduodenal diseases.…”

Section: Resultsmentioning

confidence: 91%

Risk Assessment of Gastric Cancer Caused by Helicobacter pylori Using CagA Sequence Markers

Zhang

2012

PLoS ONE

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BackgroundAs a marker of Helicobacter pylori, Cytotoxin-associated gene A (cagA) has been revealed to be the major virulence factor causing gastroduodenal diseases. However, the molecular mechanisms that underlie the development of different gastroduodenal diseases caused by cagA-positive H. pylori infection remain unknown. Current studies are limited to the evaluation of the correlation between diseases and the number of Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs in the CagA strain. To further understand the relationship between CagA sequence and its virulence to gastric cancer, we proposed a systematic entropy-based approach to identify the cancer-related residues in the intervening regions of CagA and employed a supervised machine learning method for cancer and non-cancer cases classification.MethodologyAn entropy-based calculation was used to detect key residues of CagA intervening sequences as the gastric cancer biomarker. For each residue, both combinatorial entropy and background entropy were calculated, and the entropy difference was used as the criterion for feature residue selection. The feature values were then fed into Support Vector Machines (SVM) with the Radial Basis Function (RBF) kernel, and two parameters were tuned to obtain the optimal F value by using grid search. Two other popular sequence classification methods, the BLAST and HMMER, were also applied to the same data for comparison.ConclusionOur method achieved 76% and 71% classification accuracy for Western and East Asian subtypes, respectively, which performed significantly better than BLAST and HMMER. This research indicates that small variations of amino acids in those important residues might lead to the virulence variance of CagA strains resulting in different gastroduodenal diseases. This study provides not only a useful tool to predict the correlation between the novel CagA strain and diseases, but also a general new framework for detecting biological sequence biomarkers in population studies.

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“…The metabolite M0 was eluted at 3.67 min, with an protonated [M + H] + molecular ion at m/z 295. 16, and the product ions were at m/z 195.07 and 84.08, Figure 2. Workflow of the troxipide study.…”

Section: Resultsmentioning

confidence: 99%

Metabolites profiling and pharmacokinetics of troxipide and its pharmacodynamics in rats with gastric ulcer

Guo

Chen

Yan

et al. 2020

Sci Rep

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Troxipide is widely used to treat gastric ulcer (GU) in the clinic. However, a lack of systematic metabolic, pharmacokinetic and pharmacological studies limits its clinical use. This study aimed to firstly explore the metabolic, pharmacokinetic and pharmacological mechanisms of troxipide in rats with GU compared to normal control (NC) rats. First, metabolic study was perormed by a highly selective, high-resolution mass spectrometry method. A total of 45 metabolites, including 9 phase I metabolites and 36 phase II metabolites, were identified based on MS/MS spectra. Subsequently, the pharmacokinetics results suggested that the C max , K a , t 1/2 , AUC (0−t) and AUC (0−∞) of troxipide were significantly increased in rats with GU compared with NC rats. The V z , K 10 and absolute bioavailability of troxipide were obviously decreased in rats with GU compared with NC rats, and its tissue distribution (in the liver, lung and kidney) was significantly different between the two groups of rats. Additionally, the pharmacodynamic results suggested that the levels of biochemical factors (IL-17, IL-6, TNF-α, IFN-γ, AP-1, MTL, GAS, and PG-II) were significantly increased, the PG-Ӏ level was obviously decreased, and the protein expression levels of HSP-90, C-Cas-3 and C-PARP-1 were markedly increased in rats with GU compared with NC rats. The above results suggested that the therapeutic mechanisms underlying the metabolic, pharmacokinetic and pharmacological properties of troxipide in vivo in rats deserve further attention based on the importance of troxipide in the treatment of GU in this study, and these mechanisms could be targets for future studies. Gastric ulcer, (GU) a common disease in the clinic, is a peptic ulcer that affects humans of all ages. It is associated with morbidity and mortality, and has become a medical-social problem of global importance that has received increased attention 1-4. The frequent occurrence of GU between the cardia and pylorus mainly results form tissue damage caused by digestive juices decomposing the gastric mucosa, especially near the lesser curvature of the stomach and gastric antrum 5-8. Currently, GU is a widely considered multifactorial disease because it is related to gastric acid, gastric pepsin, infection, physical fitness, environment, living habits and so on 9-11. If not treated adequately, GU can lead to serious complications such as perforation and bleeding 12-15. In addition, the acetic acid-induced GU in rats is most similar to GU in humans 16-20. Here, acetic acid-induced GU is more severe than other GU models (ethanol-, ligation-and reserpine-induced models), and is the most commonly used model for experimental research on GU 21,22. Moreover,this model is reproducible and reliable. Therefore, we selected a rat model of GU to evaluate relative studies of troxipide in the paper. Troxipide (3,4,5-trimethoxy-N-3-piperidinyl, Fig. 1), a defensive factor-enhancing therapeutic agent for gastritis and GU that exerts inhibitory, therapeutic and preventive effects to specifically tho...

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The Risk of Gastric Cancer in Patients with Duodenal and Gastric Ulcer: Research Progresses and Clinical Implications

Cited by 9 publications

References 72 publications

Differential Proteomics of Helicobacter pylori Associated with Autoimmune Atrophic Gastritis

Differential Proteomics of Helicobacter pylori Associated with Autoimmune Atrophic Gastritis

Risk Assessment of Gastric Cancer Caused by Helicobacter pylori Using CagA Sequence Markers

Metabolites profiling and pharmacokinetics of troxipide and its pharmacodynamics in rats with gastric ulcer

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