International journal of gastrointestinal cancer · 2005
Gastric mucosal proliferative and total tyrosine kinases activities increase in Helicobacter pylori-induced chronic gastritis.
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Kotynia Justyna, Kordek Radzislaw, Kozlowska Alicja, Malecka-Panas Ewa
Аннотация
BACKGROUND: The intestinal type of gastric cancer is thought to originate from cancer precursor lesions, progressing from H. pylori-induced chronic gastritis, atrophic gastritis, to intestinal metaplasia (IM) and dysplasia. Tyrosine kinases (tyr-k) represent the family of proteins that are widely expressed during cell metabolism and are considered as secondary markers for cellular proliferation and malignant transformation.
AIM OF STUDY: The aim of the study was to evaluate the correlation between gastric mucosal histopathologic changes, total tyrosine kinases, and proliferative activities in patients with H. pylori infection.
METHODS: Biopsy specimens from the gastric mucosa of 94 patients were assessed for H. pylori infection, histopathology (according to the Sydney classification), proliferative activity [Ki-67 immunohistochemistry with labeling index (LI) estimation], and total tyr-k activities (ELISA assay kit).
RESULTS: Total tyr-k activities and Ki-67 LI were significantly higher in H. pylori (+) than H. pylori (-) group (728.1 +/- 175.3 vs 360.1 +/- 44.4 pmol P/mg/min. p <0,01 and 20.0 +/- 5.8 vs 10.9 +/- 1.3 %, respectively). A significant correlation has been observed between the Ki-67 LI and total tyr-k activities in patients with and without H. pylori infection. In cases of gastritis accompanied with atrophic changes or intestinal metaplasia in H. pylori (+) patients, Ki-67 LI and total tyr-k activities were particularly high compared to chronic gastritis without atrophy or intestinal metaplasia.
CONCLUSION: Those results suggest that tyrosine kinases may play an important role in the development of gastric mucosal hyperproliferation in H. pylori-induced gastritis and possibly in early phase of gastric carcinogenesis.
AIM OF STUDY: The aim of the study was to evaluate the correlation between gastric mucosal histopathologic changes, total tyrosine kinases, and proliferative activities in patients with H. pylori infection.
METHODS: Biopsy specimens from the gastric mucosa of 94 patients were assessed for H. pylori infection, histopathology (according to the Sydney classification), proliferative activity [Ki-67 immunohistochemistry with labeling index (LI) estimation], and total tyr-k activities (ELISA assay kit).
RESULTS: Total tyr-k activities and Ki-67 LI were significantly higher in H. pylori (+) than H. pylori (-) group (728.1 +/- 175.3 vs 360.1 +/- 44.4 pmol P/mg/min. p <0,01 and 20.0 +/- 5.8 vs 10.9 +/- 1.3 %, respectively). A significant correlation has been observed between the Ki-67 LI and total tyr-k activities in patients with and without H. pylori infection. In cases of gastritis accompanied with atrophic changes or intestinal metaplasia in H. pylori (+) patients, Ki-67 LI and total tyr-k activities were particularly high compared to chronic gastritis without atrophy or intestinal metaplasia.
CONCLUSION: Those results suggest that tyrosine kinases may play an important role in the development of gastric mucosal hyperproliferation in H. pylori-induced gastritis and possibly in early phase of gastric carcinogenesis.