Endoscopic resection appears to be a safe and effective treatment for duodenal carcinoid tumors measuring ≤ 10 mm in diameter and confined to the submucosal layer.
Clinicopathological features associated with young gastric cancer include upper location, linitis plastica, histopathologically diffuse type, and unresectability.
This nation-wide seroprevalence of H. pylori infection in South Korea was 46.6%, which showed the transition from a developing country to a developed country. More studies on the epidemiological factors and the route of transmission of H. pylori infection should be warranted.
Background Several studies have shown that the neutrophil to lymphocyte ratio (NLR) in peripheral blood is a prognostic factor of various cancers. However, there is limited information on the clinical and prognostic significance of NLR in patients with metastatic advanced gastric cancer (AGC). Therefore, we examined whether the NLR can be used as a prognostic marker for predicting chemotherapeutic response and survival outcomes in metastatic AGC patients who are receiving palliative chemotherapy. Method A total of 268 patients diagnosed with metastatic AGC were enrolled. NLR was calculated from complete blood cell count taken before the first chemotherapy treatment. Patients were divided into two groups according to the median value of NLR: a high NLR group and a low NLR group. Result The median follow-up period was 340 days (range 72-1796 days) and median NLR was 3.06 (range 0.18-18.16). The high NLR group (NLR [3.0) contained 138 patients and the low NLR group (NLR B3.0) contained 130 patients. Low NLR group patients had a significantly higher chemotherapeutic disease control rate (90.0 % vs. 80.4; P = 0.028), and longer progression-free survival (PFS) and overall survival (OS) than the high NLR group patients (186 vs. 146 days; P = 0.001; 414 vs. 280 days; P \ 0.001, respectively). In multivariate analysis, NLR showed a significant association with PFS (HR 1.478; 95 % CI 1.154-1.892; P = 0.002) and OS (HR 1.569; 95 % CI 1.227-2.006; P \ 0.001). Conclusion Pretreatment NLR is a useful prognostic marker in patients with metastatic AGC who are undergoing palliative chemotherapy.
The Helicobacter pylori protein CagA may undergo tyrosine phosphorylation following its entry into human gastric epithelial cells with downstream effects on signal transduction. Disruption of the gp130 receptor that modulates the balance of the SHP2/ERK and JAK/STAT pathways enhanced peptic ulceration and gastric cancer in gp130 knock-out mice. In this study, we evaluated the effect of translocated CagA in relation to its tyrosine phosphorylation status on the gp130-mediated signal switch between the SHP2/ERK and JAK/STAT3 pathways. We showed that in the presence of CagA, SHP2 was recruited to gp130. Phosphorylated CagA showed enhanced SHP2 binding activity and ERK1/2 phosphorylation, whereas unphosphorylated CagA showed preferential STAT3 activation. These findings indicate that the phosphorylation status of CagA affects the signal switch between the SHP2/ERK and JAK/STAT3 pathways through gp130, providing a novel mechanism to explain H. pylori signaling.Helicobacter pylori frequently colonizes the human stomach (1), and hosts infected by cagA-positive strains are at increased risk of gastric cancer and peptic ulceration (2-10). H. pylori injects the CagA protein into host gastric epithelial cells via a type IV secretion system (11-16). The injected CagA is tyrosine-phosphorylated by Src family protein-tyrosine kinases and binds SHP2 (Src homology 2 domain-containing Src homology tyrosine phosphatase) (17-21); the CagA-SHP2 complex has been detected in human gastric mucosa (22,23).The IL6/gp130/STAT3 (interleukin-6/glycoprotein 130/signal transducer and activation of transcription 3) pathway has been shown to play a role in the development of gastric cancer (24, 25). IL6 exerts its biological activities through the receptor subunit gp130 (26). At least two functional modules of gp130 have been characterized; one encompasses four membranedistal Tyr(P) binding sites for the Src homology 2 domain of the latent transcription factors, STAT1 and STAT3. The other comprises the membrane-proximal Tyr(P) 757 residue responsible for the engagement of cytoplasmic SHP2 (26, 27).IL6 induces recruitment and homodimerization of gp130, potentially leading to balanced signaling through both the JAK/ STAT and SHP2/Ras/ERK signaling pathways (28, 29). However, disrupting this balance in the gp130 "knock-in" mouse induced premalignant lesions, including atrophy, intestinal metaplasia, dysplasia, and ultimately gastric cancer (24). Similarly, when the IL6 cytokine family signaling pathway is disrupted, increased STAT3 signaling may favor development of gastric adenomas, whereas increased SHP2/ERK 2 signaling may lead to mucosal inflammation (25,30).That cellular factors that are up-regulated in response to H. pylori could modulate SHP2/ERK or JAK/STAT signaling pathways suggests that H. pylori persistence and its consequent pathologies could be influenced by gp130-mediated signal transduction through these pathways (30). In this study, we examined the role of CagA tyrosine phosphorylation status in the activation of the SHP2/ERK and...
SummaryTo determine the effect of Helicobacter pylori CagA expression on interleukin-8 (IL-8) induction in AGS cells, cagA and five of its fragments from strains 147A and 147C that vary in the 3 ′ ′ ′ ′ repeat region were cloned into the eukaryotic expression plasmid pSP65SR α α α α . IL-8, but not RANTES or IL-I β β β β , levels were increased in AGS cells transfected with 147A-cagA and to a greater extent with 147C-cagA , compared with negative controls. The 5 ′ ′ ′ ′ b fragment from the two strains had similar effects, but the 3 ′ ′ ′ ′ d and e fragments from 147C CagA had greater effects than those from 147A-CagA. When the Western CagA-specific sequence (WSS) of 147C-cagA was replaced with East Asian CagA-specific sequence (ESS) and cloned into pSP65SR α α α α as an East/West chimera, there was no significant effect on IL-8 production. Use of specific inhibitors indicates that Src kinase activation, and the mitogen-activated protein (MAP) kinase and NF-κ κ κ κ B pathways are the major intermediates for CagA effects on IL-8 induction, but the p38 MAP kinase pathway has little effect. These results indicate a direct CagA effect on IL-8 induction by gastric epithelial cells, and indicate signal pathway loci that can be targeted for amelioration.
Helicobacter pylori
infection is one of the most common infectious diseases worldwide. Although the prevalence of
H. pylori
is gradually decreasing, approximately half of the world's population still becomes infected with this disease.
H. pylori
is responsible for substantial gastrointestinal morbidity worldwide, with a high disease burden. It is the most common cause of gastric and duodenal ulcers and gastric cancer. Since the revision of the
H. pylori
clinical practice guidelines in 2013 in Korea, the eradication rate of
H. pylori
has gradually decreased with the use of a clarithromycin-based triple therapy for 7 days. According to a nationwide randomized controlled study conducted by the Korean College of
Helicobacter
and Upper Gastrointestinal Research released in 2018, the intention-to-treat eradication rate was only 63.9%, which was mostly due to increased antimicrobial resistance, especially from clarithromycin. The clinical practice guidelines for the treatment of
H. pylori
were updated according to evidence-based medicine from a meta-analysis conducted on a target group receiving the latest level of eradication therapy. The draft recommendations developed based on the meta-analysis were finalized after an expert consensus on three recommendations regarding the indication for treatment and eight recommendations for the treatment itself. These guidelines were designed to provide clinical evidence for the treatment (including primary care treatment) of
H. pylori
infection to patients, nurses, medical school students, policymakers, and clinicians. These may differ from current medical insurance standards and will be revised if more evidence emerges in the future.
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