Apoptotic cell death and its relationship to gastric carcinogenesis
Autor: | A. Cevik Tufan, Nese Calli-Demirkan, N. Lale Satiroglu-Tufan, Metin Akbulut, Ferda Bir |
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Rok vydání: | 2007 |
Předmět: |
p53
Pathology Intestinal metaplasia protein p53 tissue distribution Chronic gastritis Apoptosis Gastroenterology stomach adenocarcinoma Metaplasia bcl-2-Associated X Protein TUNEL assay biology adult TUNEL staining digestive oral and skin physiology article General Medicine Middle Aged protein function aged female medicine.anatomical_structure Proto-Oncogene Proteins c-bcl-2 immunohistochemistry cytoplasm histopathology Immunohistochemistry Adult Aged Female Gastric Mucosa/pathology Humans In Situ Nick-End Labeling Male Proto-Oncogene Proteins c-bcl-2/analysis Stomach Neoplasms/chemistry/*pathology Tumor Suppressor Protein p53/analysis bcl-2-Associated X Protein/analysis medicine.symptom protein Bax malignant transformation medicine.medical_specialty protein bcl 2 regulatory mechanism nick end labeling Bcl-2-associated X protein male Stomach Neoplasms Internal medicine medicine Gastric mucosa Bcl-2 controlled study human bax bcl-2 intestinal metaplasia apoptosis protein expression stomach carcinogenesis gastric cancer gastritis Cancer medicine.disease cancer classification major clinical study human tissue digestive system diseases Gastric Mucosa Bax protein analysis chronic gastritis intestine metaplasia biology.protein Tumor Suppressor Protein p53 Gastric cancer stomach carcinoma |
Zdroj: | Europe PubMed Central |
ISSN: | 1007-9327 |
Popis: | Aim: To investigate the apoptotic process of cells within the intestinal metaplasia areas co-localizing with chronic gastritis and gastric carcinomas and to analyze the involvement of proteins regulating apoptosis in the process of intestinal metaplasia related gastric carcinogenesis. Methods: Forty-two gastric carcinoma and seventeen chronic gastritis cases were included in this study. All cases were examined for the existence of intestinal metaplasia. Ten cases randomly selected from each group were processed for TUNEL assay. TUNEL positive cells within the intestinal metaplasia areas, colocalizing either to gastric carcinoma or chronic gastritis, were counted and converted to apoptotic indices. In addition, p53, bcl-2 and bax expression patterns within these tissues were analyzed on the basis of immunohistochemistry. Results: Twenty-eight of the cases were intestinal and 14 of the cases were diffuse type adenocarcinomas. 64% (27/42) of the gastric carcinoma cases had intestinal metaplasia. Intestinal metaplasia co-localized more with intestinal type carcinomas compared with diffuse type carcinomas [75% (21/28) vs 42% (6/14), respectively; P ≤ 0.05]. The mean apoptotic index in tumor cells was 0.70 ± 0.08. The mean apoptotic index in intestinal metaplasias co-localizing to tumors was significantly higher than that of intestinal metaplasias co-localizing to chronic gastritis (0.70 ± 0.03 vs 0.09 ± 0.01, respectively; P ≤ 0.05). p53 positivity was not observed in areas of intestinal metaplasia adjacent to tumors or chronic gastritis. Intestinal metaplasia areas adjacent to tumors showed lower cytoplasmic bcl-2 positivity compared to intestinal metaplasia areas adjacent to chronic gastritis [55.5% (15/27) vs 70.5% (12/17), respectively]. On the other hand, intestinal metaplasia areas adjacent to tumors showed significantly higher cytoplasmic bax positivity compared to intestinal metaplasia areas adjacent to chronic gastritis [44.4% (12/27) vs 11.7% (2/17), respectively; P ≤ 0.05]. Conclusion: Existence of apoptotic cells on the basis of TUNEL positivity is shown in intestinal metaplasias co-localizing to both diffuse and intestinal type gastric cancers in this study. Our results also suggested bax expression dependent induction of apoptosis especially in intestinal metaplasia areas adjacent to tumors. These findings strongly support the involvement of apoptotic mechanisms in the process of gastric carcinogenesis especially in the transition from intestinal metaplasia to gastric cancer. It may be suggested that induction of apoptosis in intestinal metaplasia areas adjacent to tumors may involve different mechanisms than induction by chronic inflammation. © 2007 The WJG Press. All rights reserved. |
Databáze: | OpenAIRE |
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