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Immunohistochemical evaluation of p53 expression and proliferative activity in children with Helicobacter pylori
Yesim Ozturk1, Erdener Ozer, Banu Lebe
1Department of Pediatric Gastroenterology and Nutrition, Dokuz Eylul University School of Medicine, Izmir, Turkey. yesim.ozturk@deu.edu.tr
Insights
p53 expression and increased cell proliferation are linked to Helicobacter pylori gastritis in children. However, these p53 alterations do not appear to initiate gastric cancer development in adulthood.
Area of Science:
- Pediatric Gastroenterology
- Oncology
- Microbiology
Background:
- Helicobacter pylori (H. pylori) infection is a common cause of gastritis in children.
- Gastritis involves inflammation of the stomach lining, potentially leading to cellular changes.
- The p53 protein plays a crucial role in cell cycle regulation and tumor suppression.
Purpose of the Study:
- To investigate the relationship between p53 expression, glandular epithelial proliferation, and intestinal metaplasia in pediatric H. pylori-associated gastritis.
- To assess the significance of these markers in the context of H. pylori infection in children.
Main Methods:
- Endoscopic gastric biopsies were obtained from 54 children with dyspeptic symptoms.
- Immunohistochemistry was used to evaluate p53 expression and Ki-67 labeling index (proliferative activity).
- Histological analysis assessed H. pylori density, intestinal metaplasia, and inflammatory cell infiltration.
Main Results:
- H. pylori infection was present in 64% of the children.
- p53 expression was observed in 20.4% of cases, with 91% of these being H. pylori positive.
- H. pylori density and Ki-67 index were positively correlated, and were significantly higher in p53-positive children.
Conclusions:
- p53 alterations and increased glandular epithelial proliferation may be associated with H. pylori-associated gastritis in pediatric patients.
- p53 mutations were not significantly associated with intestinal metaplasia, a precursor to gastric cancer in adults.
- H. pylori-associated p53 alterations are unlikely to initiate or promote gastric cancer development later in life.
Objectives:
The aim of this study was to evaluate the significance of p53 expression and proliferative activity of glandular epithelium and intestinal metaplasia in Helicobacter pylori associated gastritis of pediatric patients.
Methods:
The study included endoscopic gastric biopsies of 54 children with dyspeptic complaints. Immunohistochemistry was performed for evaluation of p53 expression and Ki-67 labeling index, an indicator of proliferative activity. Grading of H. pylori density, intestinal metaplasia and inflammatory cell infiltration were performed in histologic tissue sections stained with hematoxylin-eosin, Giemsa and Alcian-blue.
Results:
Of 54 children, 35 (64%) were infected by H. pylori. Positive immunostaining for p53 was observed in 11 of 54 cases (20.4%). H. pylori infection was found in 10 (91%) of the p53-positive patients. There was a positive correlation between H. pylori density and Ki-67 labeling index in H. pylori infected children. H. pylori density, Ki-67 labeling index and inflammatory cell infiltration in the p53-positive group were significantly higher than in the p53-negative group. Although intestinal metaplasia was more common in H. pylori infected children (n = 11; 31.4%), there was no difference in the rate of intestinal metaplasia between the p53-positive and p53-negative groups.
Conclusions:
The present study shows that p53 mutations and higher proliferative activity of glandular epithelium may be related to H. pylori associated gastritis in children. Because p53 mutation does not appear to be associated with intestinal metaplasia, a precursor for gastric cancer in adults, we think that H.pylori associated p53 alterations do not initiate and promote gastric cancer that may occur in adulthood.
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