Browsing by Subject "COX-2"

Now showing 1 - 3 of 3
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    Expression of cyclooxygenase-2 has no impact on survival in adenocarcinoma of the esophagogastric junction but is associated with favourable clinicopathologic features
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Knie, Juliana; Reddemann, Katharina; Petrova, Ekaterina; Herhahn, Tobias; Wellner, Ulrich; Thorns, Christoph
    Background. COX-2 expression induces carcinogenesis and is thought to be an adverse prognostic factor in gastric carcinomas while the prognostic value of DNA mismatch repair (MMR) is still controversial. Concerning adenocarcinomas of the esophagogastric junction, no comprehensive data regarding either factors are available as of yet. Objective. We assessed expression of COX-2, MLH1 and MSH2 in adenocarcinoma of the esophagogastric junction in relation to patients’ survival and various clinicopathologic features. Design. Immunohistochemical studies (using antibodies against COX-2, MLH1 and MSH2) were performed in a study population of 228 tumours. Followup data was available for all patients with a mean follow-up time of 42.8 months. Results. 78 (34.2%) tumours were COX-2 negative, 148 (64.9%) showed COX-2 positivity. Assessment of COX-2 expression and clinicopathologic features revealed an inverse correlation with depth of tumour invasion and number of metastatic lymph nodes (p=0,021 and p=0,004, respectively). No correlation with other features could be demonstrated. 62 cases (27.2%) showed loss of DNA repair enzymes MLH1 and/or MSH2. MMR differed significantly between COX-2 positive and negative cases (p=0,028). KaplanMeier survival analyses revealed no impact on patients’ survival for COX-2 expression or MMR status (p=0.837 and p=0.972, respectively). Conclusions. Expression of COX-2 in adenocarcinomas of the esophagogastric junction seems to have no prognostic effect or impact on patients’ survival but is associated with favourable clinico-pathologic factors. MMR deficiency was more frequent in COX-2 negative tumours, but MMR status had no impact on survival and patients’ outcome whatsoever
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    Helicobacter pylori vacA affects the expression of COX-2 in the duodenal mucosa of patients with duodenitis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Chu, Yan; Chen, Fengyuan; Pan, Qincong; Cheng, Nuo; Liu, Xiuping; Feng, Jie
    Duodenitis refers to inflammation that occurs in the duodenum. Helicobacter pylori (Hp) is a known risk factor for duodenitis. This paper attempted to analyze the correlation between Hp virulence genotypes and the initiation and development of duodenal bulbar inflammation (DBI) to lay the foundation for the management of duodenitis induced by Hp infection. Total RNA was extracted from duodenal samples of 156 Hp-positive patients [70 with DBI and 86 with duodenal bulbar ulcer (DBU)] and 80 Hp-free DBI patients, followed by RT-qPCR detection of COX-2 mRNA expression and the presence of virulence factors. The cagA positive (62.2%), vacAs1 (21.79%), vacAm2 (23.72%), vacAs1m2 (19.87%) and iceA1 (55.80%) genotypes were dominant in 156 Hp-positive samples. Statistical difference was observed in vacAs and vacA mixtures between DBI and DBU patients. Gastric metaplasia had an association with vacA allelotypes, and its occurrence had strong correlations with vacAs1 and vacAs1m2 genotypes. The vacAs1 and vacAs1m2 genotypes were correlated with gastric metaplasia occurrence (all p<0.05). There were significant correlations between vacAs and vacA mixtures with cagA genotypes, and between iceA genotypes with vacA mixtures (all p<0.05). COX-2 was strongly expressed in Hp-infected duodenal mucosa and showed correlations with vacA genotype. COX-2 was differentially expressed in vacAs1- and vacAs2-positive patients. COX-2 was more highly upregulated in vacAs1m1- and vacAs1m2-positive patients than vacAs2m2-positive patients. Overall, Hp virulence genotype vacA was correlated with DBI and DBU initiation and development.
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    Mechanism of Weiwei granules in the treatment of chronic active Helicobacter pylori gastritis with atrophy based on the TLR4/NF-κB/COX-2 inflammatory signaling pathway
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Zhang, Haipeng; Liu, Hongyan
    Objective. Our paper aimed to elucidate the mechanism of Weiwei granules in the treatment of Helicobacter pylori (Hp)-positive chronic atrophic gastritis (CAG) based on the TLR4/NF-κB/COX-2 inflammatory signaling pathway. Methods. Hp-positive CAG patients were randomized into the control group (treated with quadruple therapy) or the observation group (treated with Weiwei granules based on the control group). The clinical efficacy, Hp clearance rate, and efficacy of traditional Chinese medicine (TCM) symptoms were compared between the two groups after six months of treatment. The scores of various histopathology variables, serum levels of inflammatory factors (interleukin-6 [IL-6], interleukin-8 [IL-8], and tumor necrosis factor-alpha [TNF-α]), gastrin-17 (G-17) and motilin (MTL), pepsinogen (PG) I and PG II, as well as serum levels of gastrointestinal hormone endothelin (ET), epidermal growth factor (EGF), and calcitonin gene-related peptide (CGRP), were compared between the two groups before and after treatment. TLR4, NF-κB, and COX-2 mRNA levels were compared in gastric mucosal tissues before and after treatment in the two groups. Results. After treatment, the clinical efficacy, Hp clearance rate, and efficacy of TCM symptoms of patients in the observation group were higher than those in the control group. After treatment, the scores of various histopathology variables, serum levels of inflammatory factors (IL-6, IL-8, and TNF-α), gastrointestinal hormones (ET and EGF), and the expression levels of TLR4, NF-κB, and COX-2 mRNA in the gastric mucosal tissues were lower and G-17, MTL, CGRP, and PG I levels were higher in the observation group than in the control group. Conclusion. Weiwei granules can effectively improve Hp-positive CAG patients and reduce the expression levels of TLR4, NF-κB, and COX-2