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Sayfa 1 itibaren 106 Sonuçlar
Gastric mucosal proliferative and total tyrosine kinases activities increase in Helicobacter pylori-induced chronic gastritis.
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BACKGROUND
The intestinal type of gastric cancer is thought to originate from cancer precursor lesions, progressing from H. pylori-induced chronic gastritis, atrophic gastritis, to intestinal metaplasia (IM) and dysplasia. Tyrosine kinases (tyr-k) represent the family of proteins that are widely
Pathogenetic role of the tyrosine-phosphorylated CagA EPIYA sequence of Helicobacter pylori in histological gastritis in Japanese patients.
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BACKGROUND
Helicobacter pylori (H. pylori) CagA protein plays an important role in the clinical outcome of gastritis treatment. Tyrosine phosphorylated Glu-Pro-Ile-Tyr-Ala motif in CagA (CagA-P) plays a critical role in the morphological transformation of cells.
OBJECTIVE
We examine the relationship
The number of Helicobacter pylori CagA EPIYA C tyrosine phosphorylation motifs influences the pattern of gastritis and the development of gastric carcinoma.
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OBJECTIVE
To characterize the variation in virulence of Helicobacter pylori associated with CagA Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs, and to explore its relationship with the histopathological features of chronic gastritis and with the development of gastric carcinoma.
RESULTS
A total of 169 H.
Necrotizing Hemorrhagic Gastritis following Acute Myeloid Leukemia Induction with Midostaurin: An Unexpected Complication.
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Midostaurin is a tyrosine multikinase inhibitor approved for the treatment of patients with newly diagnosed acute myeloid leukemia (AML) with mutated Fms-like tyrosine kinase-3. We describe a case report of a 49-year-old AML patient treated with an intensive chemotherapy regimen followed by
Deregulation of SHP-2 tyrosine phosphatase by the Helicobacter pylori virulence factor CagA.
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Helicobacter pylori (H. pylori) is estimated to infect about half of the world population. It causes gastric diseases ranging from gastritis to cancer and has been classified as a class I carcinogen by WHO. However, little is known about the molecular mechanisms by which H. pylori induces
Protein tyrosine phosphatase beta, a receptor for Helicobacter pylori vacA toxin.
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Helicobacter pylori is the leading bacterial cause of food-borne illness worldwide and plays a major role in the development of chronic gastritis, peptic ulcer, and gastric cancer. Strains isolated from patients contain the cagA gene (cytotoxin-associated gene A) and produce the vacuolating
Relationship between Helicobacter pylori tyrosine-phosphorylated CagA-related markers and the development of diffuse-type gastric cancers: a case-control study.
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OBJECTIVE
Tyrosine phosphorylation of the EPIYA motif in Helicobacter pylori CagA (CagA-P) plays an important role in toxic reaction. Diffuse-type gastric cancer (DGC) has a poor prognosis. We tried to clarify the expression level of CagA-P in DGC patients.
METHODS
We enrolled 42 early-stage DGC
Association between diversity in the Src homology 2 domain--containing tyrosine phosphatase binding site of Helicobacter pylori CagA protein and gastric atrophy and cancer.
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We investigated the relationship between the diversity of Helicobacter pylori CagA protein and clinical outcome. The cagA gene was sequenced in 115 clinical isolates. The binding affinity of CagA to Src homology 2 domain-containing tyrosine phosphatase (SHP-2) was examined by in vitro infection. Two
Water extract of Helicobacter pylori stimulates interleukin-8 secretion by a human gastric epithelial cell line (JR-St) through protein tyrosine phosphorylation.
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BACKGROUND
Infection by Helicobacter pylori induces cytokine production in gastric mucosal cells. Production of interleukin-8 (IL-8) is known to be markedly increased and is believed to play an important role in gastric mucosal inflammation. The aim of this study was to elucidate the effects of
Application of PCR amplicon sequencing using a single primer pair in PCR amplification to assess variations in Helicobacter pylori CagA EPIYA tyrosine phosphorylation motifs.
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BACKGROUND
The presence of various EPIYA tyrosine phosphorylation motifs in the CagA protein of Helicobacter pylori has been suggested to contribute to pathogenesis in adults. In this study, a unique PCR assay and sequencing strategy was developed to establish the number and variation of cagA EPIYA
Composition and gene expression of the cag pathogenicity island in Helicobacter pylori strains isolated from gastric carcinoma and gastritis patients in Costa Rica.
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The composition and in vitro expression of the cag pathogenicity island genes in a group of Helicobacter pylori strains obtained from patients suffering from chronic gastritis-associated dyspepsia (n = 26) or gastric carcinoma (n = 17) were analyzed. No significant difference in the distribution of
Stimulation of IL-8 production in human gastric epithelial cells by Helicobacter pylori, IL-1beta and TNF-alpha requires tyrosine kinase activity, but not protein kinase C.
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Production of interleukin 8 (IL-8) is believed to be important in the pathogenesis of the gastritis seen in Helicobacter pylori infection. The aim of this study was to investigate the roles of protein kinase A (PKA), protein kinase C (PKC), protein tyrosine kinase (PTK) and intracellular calcium in
CagA tyrosine phosphorylation in gastric epithelial cells caused by Helicobacter pylori in patients with gastric adenocarcinoma.
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BACKGROUND
Tyrosine phosphorylation of Helicobacter pylori cytotoxin-associated protein of in gastric epithelial cells is reported. The goals of this study are first to examine the occurrence of CagA tyrosine phosphorylation in H. pylori strains isolated from patients with gastric adenocarcinoma and
The Influence of Prolonged Acetylsalicylic Acid Supplementation-Induced Gastritis on the Neurochemistry of the Sympathetic Neurons Supplying Prepyloric Region of the Porcine Stomach.
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This experiment was designed to establish the localization and neurochemical phenotyping of sympathetic neurons supplying prepyloric area of the porcine stomach in a physiological state and during acetylsalicylic acid (ASA) induced gastritis. In order to localize the sympathetic perikarya the
[Gastric carcinoma and chronic gastritis: epigenetic regulation of CDH1 (E-Cadherin), CDKN2A (p16INK4A), PTGS2 (COX-2) and EGFR genes through methylation].
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The genetic and epigenetic alterations are being studied as one of the causes of gastric cancer (GC) progression and development. DNA methylation is an epigenetic alteration which leads to suppressor gene silencing and proto-oncogene activation, playing an important role in carcinogenesis. The
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