Gastric mucosal proliferative and total tyrosine kinases activities increase in Helicobacter pylori-induced chronic gastritis.

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.