Background/aims: The risk of gastric cancer is increased in patients with intestinal metaplasia. Cyclooxygenase-2 activity is crucial for gastric cancer cell survival and proliferation. We aimed to assess cyclooxygenase-2 expression in patients with intestinal metaplasia or chronic active gastritis and in patients with or without a family history of gastric cancer, i.e. a first-degree relative with gastric cancer.
Materials And Methods: One hundred and six patients with histologically proven intestinal metaplasia, chronic active gastritis or normal gastric mucosa were included. Immunohistochemical staining was performed using the immunoperoxidase method.
Results: Cyclooxygenase-2 expression was detected in 23.1% of normal gastric mucosa, 70.6% of chronic active gastritis, and 90.5% of intestinal metaplasia patients. Cyclooxygenase-2 expression was significantly higher in intestinal metaplasia than in chronic active gastritis (p=0.018). Cyclooxygenase-2 expression was significantly more severe in the intestinal metaplasia group when compared to the chronic active gastritis group (p=0.017). Severe cyclooxygenase-2 expression (>60% of cells) was more frequent in the intestinal metaplasia group. Cyclooxygenase-2 expression was higher in the Helicobacter pylori-positive group when compared to the Helicobacter pylori-negative group (80.3% vs 57.1%, respectively; p=0.012). Cyclooxygenase-2 expression did not significantly differ according to presence of a first-degree relative with gastric cancer.
Conclusions: Patients with intestinal metaplasia demonstrated increased presence and severity of cyclooxygenase-2 expression. Our findings suggest that cyclooxygenase-2 plays an important role in the stepwise process that eventually leads to gastric cancer. There was no statistically significant difference between the patients with and without a first-degree relative with a history of gastric cancer in terms of cyclooxygenase-2 expression.
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http://dx.doi.org/10.4318/tjg.2012.0432 | DOI Listing |
Front Oncol
January 2025
School of Medicine, Razi Hospital, Ilam University of Medical Sciences, Ilam, Iran.
() infection is a typical microbial agent that interferes with the complex mechanisms of gastric homeostasis by disrupting the balance between the host gastric microbiota and mucosa-related factors, ultimately leading to inflammatory changes, dysbiosis, and gastric cancer (GC). We searched this field on the basis of PubMed, Google Scholar, Web of Science, and Scopus databases. Most studies show that inhibits the colonization of other bacteria, resulting in a less variety of bacteria in the gastrointestinal (GI) tract.
View Article and Find Full Text PDFMicroorganisms
January 2025
Division of Gastroenterology, Department of Internal Medicine and Gastrointestinal Cancer Center, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul 03181, Republic of Korea.
Studies on the gastric microbiota associated with gastric precancerous lesions remain limited. This study aimed to profile the gastric mucosal microbiota in patients with -negative precancerous lesions. Gastric mucosal samples were obtained from 67 -negative patients, including those with chronic gastritis (CG), intestinal metaplasia (IM), and dysplasia.
View Article and Find Full Text PDFBiomedicines
December 2024
Department of Environmental Microbiology, School of Earth and Environmental Sciences, Babasaheb Bhimrao Ambedkar University, Vidya Vihar, Raebareli Road, Lucknow 226025, India.
The role of microbiota in human health and disease is becoming increasingly clear as a result of modern microbiome studies in recent decades. The gastrointestinal tract is the major habitat for microbiota in the human body. This microbiota comprises several trillion microorganisms, which is equivalent to almost ten times the total number of cells of the human host.
View Article and Find Full Text PDFJ Health Popul Nutr
January 2025
Department of Gastroenterology, The Affiliated Hospital of Xuzhou Medical University, Huaihai West Road, Xuzhou, Jiang Su, 221004, China.
Aims: This study aims to assess the serum levels of pepsinogen (PG)I, PG II, and gastrin (G17) in patients with gastric intestinal metaplasia (GIM) and evaluate their correlation with demographic characteristics.
Methods: A total of 247 normal controls (NC) and 240 patients diagnosed with GIM were enrolled in this study. All participants underwent a gastroscopy procedure followed by pathological examination for diagnosis confirmation.
QJM
January 2025
Peking University Traditional Chinese Medicine Clinical Medical School (Xiyuan), Peking University Health Science Center, Beijing, 100091, China.
Autoimmune gastritis (AIG) is a chronic inflammatory condition characterized by immune-mediated destruction of gastric parietal cells, leading to oxyntic atrophy, achlorhydria, and hypergastrinemia. While AIG was historically linked to gastric adenocarcinoma and type I neuroendocrine tumors (NETs), recent evidence suggests the risk of adenocarcinoma in AIG is lower than previously believed, particularly in Helicobacter pylori (H. pylori)-negative patients.
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