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Vascular endothelial growth factor-C (VEGF-C) and its receptor, vascular endothelial growth factor receptor-3 (VEGFR-3), have been implicated as important factors in the formation of lymphatic vessels, but its role in osteosarcomas has not yet been fully investigated. This study aims to define the expression of VEGF-C and VEGFR-3 in primary and metastatic osteosarcomas and their relationship to various clinicopathologic parameters. Thirty-three primary osteosarcomas and two pulmonary metastatic samples were immunostained for VEGF-C and VEGFR-3. In addition, VEGF-C and vascular endothelial growth factor-D (VEGF-D) mRNA expression levels in three different human osteosarcoma cell lines and control fibroblasts were evaluated by real-time quantitative polymerase chain reaction (PCR). Both VEGF-C and VEGFR-3 were expressed mainly in the cytoplasm of the tumor cells. Of the 35 patients with osteosarcoma, 16 patients (45.7%) showed strong positive reaction with VEGF-C. Four cases (11.4%) were negative, and 15 cases (42.9%) showed weak immunoreactivity. For VEGFR-3, 12 patients (34.3%) showed strong positive reaction. Fifteen cases (42.9%) were negative, and eight cases (22.8%) showed weak immunoreactivity. A significant, positive correlation (Rs=0.42, p=0.01) was found between the expression of VEGF-C and VEGFR-3 in osteosarcomas. The expression of VEGF-C was significantly associated with the osteoblastic subtype and high histologic grade in osteosarcomas. However, the expression of VEGF-C showed no significant correlation with the presence of metastasis. Expression of VEGFR-3 was not related to any clinicopathologic features analyzed. Two of the three osteosarcoma cell lines tested showed amplification of VEGF-C mRNA compared with control cells. No amplification of VEGF-D was noted in these cell lines. Our data suggest that VEGF-C and its receptor are expressed in osteosarcomas. Although the level of VEGF-C was high, it does not seem to have a direct influence on tumor metastasis in osteosarcomas.

Intramucosal Helicobacter pylori (H. pylori) has been described in biopsy tissues and culture systems. However, the association of intramucosal H. pylori with histopathologic features has not been evaluated. The purpose of this study is to investigate the relationship between intramucosal H. pylori and inflammatory reactions in H. pylori infection. In 113 randomly selected human gastric biopsies and 20 murine stomachs, which were inoculated with SSI every day for a week, immunohistochemical analysis for intramucosal H. pylori was done and correlated with histologic parameters. Electron microscopic examination was done on murine stomachs. H. pylori infection was present in 104 gastric biopsies and 17 murine stomachs. Intraepithelial immunopositivity for H. pylori was detected in 27 of 104 (26%) biopsies and in 11 of 17 (65%) murine stomachs. Lamina proprial immunopositivity for H. pylori was present in 51 of 104 (48%) biopsies. Neutrophil-associated immunopositivity for H. pylori was observed in 22 of 90 (24%) biopsies with H. pylori chronic active gastritis. Lamina proprial and neutrophil-associated immunopositivity for H. pylori correlated significantly with the density of H. pylori and the grade of acute inflammatory reaction in H. pylori gastritis. Intramucosal location of H. pylori itself or its antigen is closely associated with acute inflammatory reactions and may play an important role in establishing a persistent infection in chronic H. pylori gastritis. Furthermore, lamina proprial and/or neutrophil-associated H. pylori appears to be more important than intraepithelial H. pylori in acute inflammatory reactions of H. pylori gastritis.