| Background: Gastric cancer is a kind of the most popular human malignant tumor, which is the first death cause of malignant tumor in China. A upgrading tendency was found after comparision of mortality between Chinese 90s'and 70s', and most of the patients died of metastasis. So there will be significant value in the research of mechanism of genesis and metastasis, as well as the methods to prevent the metastasis. There are Many explanations in the mechanism of lymph node metastasis of gastric cancer recently, among which is the function of chemokines and chemokine receptors. Chemokine is a kind of cytokine superfamily, with molecular weight between 8-10Kda, composed by 70-80 amino acids, has the chemotaxis to WBC. There are already more than 50 chemokines, and all these chemokines are divided into 4 groups: CC, CXC, C, and CX3C. Chemokine receptor belongs to G-couple protein receptor of 7 transmembrane superfamily. Chemokine along with its corresponding receptor play vital role in formation of lymph organs, lymphatic circulation, differentiation of Th1/Th2 cells, inflammation. There is more expression of IL-8 in gastric cancer tissue than in gastric mucous menbrane. IL-8 is ELR(+)-CXCL chemokine, its receptor is CXCR1, CXCR2. CCL21(SLC) has been reported that it has chemotaxis to some gastric cancer cell line with CCR7(+). And the ligands of CCR7 are CCL21 and CCL19. Our main objective is to find out the relevance between the expressions of Chemokine receptors and metastasis. Methods: We selected 59 gastric cancer cases who accepted surgery during June-August, 2004, including 40 males and 19 females, average age was 60.5±12.0 years. The specimen were divided into three groups: primary lesion, paracarcinomatous tissues(afar 6-8cm from the edge of primary lesion), lymph node with metastasis. The specimen were made into frozen sections, one section for routine HE stain, the others were fixed by acetone then stored in -20℃ refrigerator. Some time later these sections were performed immunochemical stain to detect the expression of CXCR1, CXCR2 and CCR7. Results: There were 35 cases with lymph node metastasis in total 59 cases(59.3%). The expression of CXCR1, CXCR2 and CCR7 were mainly on membrane of tumor cells, partly in cytoplasm. The expression rates of CXCR1, CXCR2 and CCR7 in primary lesion were 56.9%,60.3%,62.1% respectively. There was no significant difference of the expression of CXCR1, CXCR2 between primary lesion and paracarcinomatous tissues, lymph node with metastasis(p>0.05), the same to the expression of CCR7 in primary lesion and lymph node with metastasis(p>0.05), but CCR7 was seldom found in normal mucous membrane(5.4%). There was no significant difference between the expression of CXCR1, CXCR2 in primary lesion and tumor differentiation, lymphatic invasion, vascular invasion, invasion depth, lymph node metastasis and TNM stage. But significant difference was found between the expression of CCR7 and these factors(p<0.05). And the vital correlative factors for lymph node metastasis were lymphatic invasion, CCR7 expression, T stage, historical differentiation. Conclusion: There was no significant difference between the expression of CXCR1, CXCR2 in primary lesion and tumor differentiation,lymphatic invasion, vascular invasion, invasion depth, lymph node metastasis and TNM stage(p>0.05). But there was significant difference between the expression of CCR7 and tumor differentiation, lymphatic invasion, vascular invasion, invasion depth, lymph node metastasis and TNM stage(p>0.05), which maybe perform some effect in the metastasis of gastric caner cell. The vital correlative factors for lymph node metastasis were lymphatic invasion, CCR7 expression, T stage, tumor differentiation. And no coordination were found between CCR7 and CXCR1, CXCR2. More long–term studies are needed in determining whether the expression of CXCR1, CXCR2 and CCR7 has independent effect upon the long-term prognosis of gastric caner patient. And still other researches are needed to detect the function of CXCR1, CXCR2 and...
|
PDF Full Text Request