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KMID : 0948320050050020153
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Konyang Medical Journal
2005 Volume.5 No. 2 p.153 ~ p.158
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Intestinal Metaplasia without Distinct Atrophic Gastritis Cause Reduction in Ratio of PepsinogenⅠ/pepsinogen Ⅱ in Gastric Cancer
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Park Eun-Hee
Mok Woo-Kyun
Min Hyun-Sik
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Abstract
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Background: Gastric cancer was reported to be related to atrophic gastritis, in which the serum pepsinogen (PG) I level and the PGI/PGII ratio reduced. It is not enough to explain the changes in PGI and PGII expressions with reduction of PGI secreting mucosa caused by atrophic gastritis in gastric cancer.
Methods: Tissue specimens of normal mucosa and invasive areas of gastric cancer were obtained from surgical cases. To investigate the other causes of the change of PG I and PGII expressions in human gastric cancer, in situ hybridization for PGI and PGII and periodic-acid schiff (PAS) stain for mucin detection were performed in the gastric mucosa.
Results: PGI and PGII genes expression was detected abundantly in the mucosa of normal region in gastric cancer without distinct atrophic gastritis. PGI gene expression was significantly decreased in the mucosa of invasive area of gastric cancer without distinct atrophic gastritis. However, PGII mRNA expression did not decreased significantly in the mucosa of invasive area of cancer without distinct atrophic gastritis compared with that of normal region. Intestinal metaplasia to mucin secreting (PAS positive) cells occurred in the mucosa of invasive area of cancer accompanying distinct atrophic gastritis, where PGI gene expression was significantly decreased whereas PGII gene expression did not decrease.
Conclusions: PGI gene expression, not PGII gene, is downregulated in the mucosa of gastric cancer accompanying intestinal metaplasia, which may be another cause of the reduction in serum PGI/PGII ratio in addition to the reduction of PGI secreting mucosa by atrophic gastritis in human gastric cancer.
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KEYWORD
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pepsinogenⅠ, pepsinogen Ⅱ, atrophic gastritis, intestinal metaplasia
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