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, co-localizing 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<or=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<or=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<or=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.