Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric carcinogenesis is a complex, multistep process, which may be influenced by many factors and is the second most common type of malignancy and the second most-common cause of mortality in the word. Interleukin-1 is up-regulated in the presence of Helicobacter pylori and is important for initiating and amplifying the inflamatory response to this infection. Recently interleukin-1 polymorphisms have been associated with the development of gastric adenocarcinoma. In this study we investigated the presence of H. pylori and host genotypes that are highly associated with gastric alterations. DNA samples were extracted and PCR-RFLP was utilized for genotyping IL-1B (-511) polymorphisms, PCR-VNTR was utilized for genotyping IL-1RN, and PCR-CTPP was utilized for genotyping IL-1B (-31), the presence of H. pylori was detected by the urease test. Our results indicate a correlation between H. pylori infection and the development of gastric cancer. We did not find an association between the presence of genotype T (thymine) in bases -511 and -31 and gastric adenocarcinoma. We also did not find any association between this polymorphism and specific type of tumor (diffuse type and intestinal type).
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PMID:Interleukin-1beta polymorphisms, Helicobacter pylori infection in individuals from Northern Brazil with gastric adenocarcinoma. 1567 46

Polymorphisms of interleukin-1 (IL-1) genes have been reported to modify the risk of gastric carcinoma (GC) in Caucasians. The significance of IL-1beta gene polymorphisms was evaluated in Japanese GC patients with or without infection of Helicobacter pylori and Epstein Barr virus (EBV) with special reference to the topographic features of GC. IL-1beta gene polymorphisms at positions -511 and +3953 were evaluated by PCR-RFLP and a penta-allelic polymorphism of IL-1RA by PCR in healthy controls (n = 103) and GC (n =140; corpus 95, antrum 45). EBV-infection was determined in the neoplastic tissues by EBER1 in situ hybridization, and H. pylori infection in nonneoplastic gastric mucosa by PCR targeting of the H. pylori urease A gene. GC consisted of EBV-associated (n = 24) and EBV-negative (n = 116) patients, whereas H. pylori infection was positive in 130 cases. Among IL-1beta gene polymorphisms, genotype IL-1beta+3953 C/T was more frequent in the EBV-negative (21%) and corpus GC (23%) patients, compared to the controls (10%), respectively, although there was no genotype IL-1beta+3953 T/T in either group. Thus, the effect of IL-1beta+3953 T was statistically significant in logistic regression models adjusted for age in EBV negativity (odds ratio [OR] 2.27, 95% confidence interval [CI] 1.02-5.05) and in the corpus GC (2.70, 1.19-6.12) with highest OR 3.55 (1.54-8.23) in EBV-negative corpus GC. There was no significant influence of IL-1 gene polymorphism in EBV-associated GC, but it occurred predominantly in the corpus (24/24) compared to EBV-negative GC (71/116) (p = 0.00002). There was no correlation between H. pylori infection and IL-1 gene polymorphism in GC. The cancer risk of the gastric corpus in Japanese is influenced by IL-1beta+3953 polymorphisms. On the other hand, the risk of EBV-associated GC, which occurs predominantly in the corpus, is not influenced by this pro-inflammatory polymorphism.
Int J Cancer 2005 May 20
PMID:Cancer risk to the gastric corpus in Japanese, its correlation with interleukin-1beta gene polymorphism (+3953*T) and Epstein-Barr virus infection. 1568 13

Helicobacter pylori cagA-positive strains and host cytokine proinflammatory polymorphisms have been associated with gastric carcinoma. However, the individual role of each factor has not been evaluated yet. Our aim was to evaluate whether IL-1 gene cluster and tumor necrosis factor-alpha (TNFA)-307 polymorphisms, as well as cagA-positive status, are associated with gastric carcinoma in a non-Caucasian population by analyzing the data in logistic regression models. We evaluated 166 patients with noncardia gastric carcinoma and 541 blood donors. Among them, 702 were successfully genotyped for all cytokine studied: 166 with gastric carcinoma and 536 controls. The carcinoma patients were considered to be H. pylori-positive if culture alone or 2 among preformed urease test, stained smear or histologic section, serology, polymerase chain reaction (PCR) for ureA and urea breath test were positive. In blood donors, H. pylori status was based on enzyme-linked immunosorbent assay. The cagA status was determined by PCR or serology. IL1B-511/-31, IL1RN (interleukin-1 receptor antagonist) and TNFA-307 polymorphisms were genotyped by PCR, PCR with restriction fragment length polymorphism, or PCR with confronting 2-pair primers. We found that the IL1RN2 polymorphic allele (OR = 1.93) was associated with noncardia gastric carcinoma, even after inclusion of age, gender and cagA status in the logistic models. However, the cagA-positive status was the strongest independent factor associated with gastric carcinoma (OR = 11.89). The other polymorphisms were not significantly associated with the disease when they were evaluated in logistic models. This study provides evidence supporting the independent associations of cagA-positive H. pylori status and IL1RN polymorphisms with noncardia gastric carcinoma.
Int J Cancer 2005 Jul 10
PMID:IL1RN polymorphic gene and cagA-positive status independently increase the risk of noncardia gastric carcinoma. 1570 54

The European Helicobacter pylori Study Group (EHPSG), during the Maastricht 2-2000 Workshop, revised and updated the original guidelines on the management of Helicobacter pylori (H. pylori) infection. The present review focuses on the diagnostic approach for patients referred to the primary care as well as to the specialist. Currently, two diagnostic methods can be used to detect H. pylori: invasive (urease test, histological detection, culture, polymerase chain reaction, smear examination, string test) or non-invasive (serology, urea breath test, antigen stool assay, ''doctor's tests'') tests. These methods vary in their sensitivity and specificity, and the choice depends on the situation, for example, whether the aim is to detect infection or the success of eradication treatment. Urea breath test (UBT) and antigen stool assay are recommended from EHPSG in patients without alarm symptoms or under 45 years of age, at low risk of malignancy in the ''test and treat strategy''. Confirmation of H. pylori eradication following treatment should be tested by UBT; a stool antigen assay is the alternative if the former is not available. Important added value can be gained from other tests: histology allows evaluation of the status of the mucosa while culture allows strain typing and tests for antibiotic susceptibility.
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PMID:[The diagnosis of helicobacter pylori infection: guidelines from the Maastricht 2-2000 Consensus Report]. 1572 82

Several Helicobacter species are known to colonize the biliary tract in animals and have been identified in the gallbladder bile of a high proportion of Chilean patients with gallbladder cancer. In this study, we tried to examine the presence of Helicobacter species in the bile to know their participation in the development of extrahepatic biliary diseases. DNA was extracted from 57 bile samples from 30 patients with benign biliary diseases (cholecystolithiasis and choledochocystolithiasis), 6 malignant biliary diseases (gallbladder cancer and common bile duct cancer), and 21 nonbiliary diseases. The presence of Helicobacter genus-, H. pylori-, H. hepaticus-, and H. bilis-specific 16S rRNA genes, the H. pylori urease A gene, and the H. pylori 26K protein gene in the bile was determined by PCR and sequencing analysis. Helicobacter genus DNA (shorter amplicons, 400 bp) was statistically frequently detected in biles from 53% (16/30) and 86% (5/6) of benign and malignant biliary diseases, compared with 9% (2/21) of nonbiliary diseases, but longer amplicons (1200 bp) were not detectable in any samples. The H. pylori urease A gene (nested amplicon) was also frequently found in bile, whether benign, malignant, or control, though neither H. pylori 16S rRNA nor the 26K protein gene was detectable in any bile samples. H. bilis-16S rRNA genes were detectable in only two cases. H. hepaticus was not detectable in any samples. DNA fragments of Helicobacter species other than H. pylori, H. hepaticus, and H. bilis are commonly detectable in the bile of patients with extrahepatic biliary diseases, whether benign or malignant, implying that the Helicobacter genus may be directly or indirectly involved in the pathogenesis of these diseases.
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PMID:Helicobacter genus DNA fragments are commonly detectable in bile from patients with extrahepatic biliary diseases and associated with their pathogenesis. 1590 58

Helicobacter pylori (H. pylori) is the commonest bacterial pathogen found worldwide and more than half the world population aged 40 years and above is colonized with it. The infection rate is >95 % in some African countries. In 1994, the International Agency for Research on cancer classified H. pylori as a class I carcinogen in humans. It causes chronic active gastritis, duodenal and gastric ulcer and gastric malignancy, and is thought to be associated with coronary artery disease, cerebral stroke, vitamin B12 and iron-deficiency anaemia, etc. Therefore, non-invasive test-and-treatment strategies are widely recommended in primary care settings. Conventionally, H. pylori infection can be diagnosed by invasive techniques using an upper gastrointestinal endoscope for obtaining multiple biopsies from different sites of the stomach for RUT, culture, histological examination, polymerase chain reaction (PCR), etc. and by non-invasive tests such as Urea breath test (UBT), stool antigen test and blood serology. At present, 13/14C-UBT is considered the test of choice for confirmation of H. pylori infection. The UBT is based on the principle, that isotopically labelled urea ingested by an H. pylori--infected patient is rapidly hydrolysed by the microbial urease. The released 13/14CO2 is absorbed across the mucous layer to the gastric mucosa and hence, excreted via the systemic circulation in the breath which is collected and measured. The non-hydrolysed urea is excreted completely in the urine within 3-4 days. 13C-UBT being non-radioactive, 13C-UBT can be used in pregnant women and children, and a user's license is not required. There is still no standard protocol accepted and followed internationally for this test. Although the methods are almost similar, various laboratories/clinics use variable tracer doses, test meals, timings and methods for breath collection, and different cut-off values, which make formal validation studies necessary. This review describes the present status of the UBT and its application in the detection of H. pylori infection.
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PMID:Urea breath test for Helicobacter pylori detection: present status. 1591 72

Anastasia Black (Russian sweet pepper) of Capsicum annuum L. var. angulosum Mill. (Solanaceae) was successively extracted with hexane, acetone, methanol and 70% methanol, and the extracts were further separated into a total of twenty-three fractions by silica gel or octadecylsilane (ODS; C18) column chromatography. These extracts and fractions were investigated for their cytotoxicity, anti-human immunodeficiency virus (HIV), anti-Helicobacter pylori (H. pylori), urease inhibition and multidrug resistance (MDR) reversal activity. Some fractions of hexane and acetone extracts showed higher cytotoxic activity against three human oral tumor cell lines (squamous cell carcinoma HSC-2, HSC-3, submandibular gland carcinoma HSG) than against three normal human oral cells (gingival fibroblast HGF, pulp cell HPC, periodontal ligament fibroblast HPLF), suggesting a tumor-specific cytotoxic activity. No fractions displayed anti-HIV activity, but some hydrophobic fractions showed higher anti-H. pylori activity, urease inhibition activity and MDR reversal activity. The higher MDR activity of these fractions against MDR gene-transfected L5178 mouse lymphoma T cells may possibly be due to their higher content of carotene or polyphenol. These data suggest that Anastasia Black should be further investigated as a potent supplement for cancer chemotherapy.
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PMID:Bioactivities of anastasia black (Russian sweet pepper). 1615 35

Helicobacter pylori (Hp) infection is an important factor in human gastric disorders, including chronic active gastritis, peptic ulcers, intestinal metaplasia and cancer. Since epidemiologic studies overwhelmingly agree on a protective influence of fruits and vegetables in reducing the risk of gastric neoplasia and processed foods made from Prunus mume Sieb. et Zucc. (Japanese apricot or "Ume" in Japanese) are traditionally known for their miscellaneous medical effects, in the present study we investigated the efficacy of a fruit-juice concentrate of Japanese apricot (CJA) in the glandular stomach of Hp-infected Mongolian gerbils. Hp-inoculated gerbils were given CJA in their drinking water at concentrations of 1 and 3% for 10 weeks. The microscopic scores for gastritis and mucosal hyperplasia in the CJA groups were significantly lower than in the Hp-inoculated control group, with dose-dependence. Real-time PCR was performed to quantitate Hp by demonstrating urease A gene amount using gerbils glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene as an internal control. Average relative urease A gene dosage in the glandular stomach in the 1 and 3% CJA and Hp-inoculated control groups was 26.6 +/- 11.6% (average +/- SE), 30.3 +/- 10.5%, 100 +/- 40.9%, respectively, the fruit-juice concentrate causing significant lowering (P<0.01 and P<0.05, respectively, with 1 and 3%). These findings suggest that suppressive effects on gastric cancer development might also be expected as a result of decreased numbers of Hp and improvement of Hp-induced chronic active gastritis on administration of CJA.
Asian Pac J Cancer Prev
PMID:Suppressive effects of fruit-juice concentrate of Prunus mume Sieb. et Zucc. (Japanese apricot, Ume) on Helicobacter pylori-induced glandular stomach lesions in Mongolian gerbils. 1623 96

Helicobacter pylori is a spiral, gram-negative rod-shaped pathogen that attaches to gastric epithelial cells in the human stomach and is a causative agent of chronic active gastritis, peptic ulcer and neoplasia. H. pylori is one of the most common pathogens afflicting humans and is the major environmental factor in the development of gastric cancer increasing from 4 to 6 folds the risk of its development. Several specific virulence factors are implicated in the mechanism of H. pylori infection like the bacterial motility; the secretion of large amounts of urease; specific adhesins for the interaction between H. pylori and the gastric surface epithelium; the traslocation into gastric ephitelial cells of the cytotoxin-associated gene A (CagA), the vacuolating cytotoxin A (VacA) and the heat shock protein HspB. Adherence of H. pylori to the gastric epithelium and secretion of interleukins are believed to be an important step in the induction of active inflammation of the mucosal layer. Several studies have demonstrated that H. pylori infection induces gastric epithelial cell proliferation activating ERK and MAPK pathways and increase of mitosis and mutations. Therefore, H. pylori infection seems to increase apoptosis, implying increased gastric epithelial cell turnover. Recently, it has been shown that H. pylori-induced apoptosis in gastric epithelial cells is mediated via the CD95-receptor/ ligand system but that TRAIL also plays an important role in this regulation.
J Exp Clin Cancer Res 2005 Sep
PMID:Helicobacter pylori and gastric epithelial cells: from gastritis to cancer. 1627 May 19

Helicobacter hepaticus is a pathogen of rodents, which causes diverse enteric and hepatic inflammatory diseases and malignancies. The urease enzyme is an important colonization factor of gastric Helicobacter species like Helicobacter pylori, but little is known about the role and regulation of urease in enterohepatic Helicobacter species. Here it is reported that urease activity of H. hepaticus does not contribute to acid resistance, and that it is nickel-responsive at the post-translational level. H. hepaticus strain ATCC 51449 did not grow or survive at pH 3.0, and supplementation with urea or NiCl2 did not abrogate this acid sensitivity. Furthermore, urease enzyme activity of H. hepaticus was acid-independent, which contrasts with the acid-induced urease system of H. pylori. Nickel supplementation of Brucella medium resulted in a tenfold increase in urease activity in both H. hepaticus and H. pylori, but the maximum level of urease activity in H. hepaticus was still three- to fivefold lower when compared to H. pylori in the same conditions. The increase in urease activity of H. hepaticus was not associated with elevation of urease mRNA or protein levels. Inhibition of protein synthesis by chloramphenicol did not affect nickel-responsive induction of urease activity in H. hepaticus, and confirmed that nickel induction occurs at the post-translational level, probably by activation of preformed apo-enzyme. In conclusion, both the role of the urease enzyme and the regulation of urease activity differ between the enterohepatic pathogen H. hepaticus and the gastric pathogen H. pylori.
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PMID:Differential regulation of urease activity in Helicobacter hepaticus and Helicobacter pylori. 1633 43


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