High levels of arginase have been detected in gastric adenocarcinoma. To examine the hypothesis that this is due to macrophage infiltration into the tumour, we localized the cellular distribution of arginase by immunohistochemical staining. We examined gastric adenocarcinomas and their corresponding normal tissues (n = 45), leiomyomas (n = 2), leiomyosarcomas (n = 3), human gastric adenocarcinoma cell lines (n = 3), and benign gastric ulcers (n = 4) by the avidin-biotin-peroxidase complex technique. Macrophages with strong arginase immunoreactivity were observed infiltrating both gastric normal and cancer tissues. No arginase immunoreactivity was observed in normal mucosal gland, muscular and serosal tissues or benign gastric ulcers. The immunoreactivity of arginase was positive but heterogeneous in most specimens of gastric adenocarcinoma (62.2%) and was absent from gastric intestinal metaplasia, leiomyomas and leiomyosarcomas. Among the 28 neoplasms with arginase immunoreactivity, scattered immunoreactivity was also noted in adjacent dysplastic glands in 12 (42.8%) specimens. Arginase immunoreactivity was observed in all three gastric cancer cell lines. Arginase is present in the cytoplasm but not in the nucleus. These data suggest that the high arginase levels in adenocarcinoma cancer tissues originate largely from cancer cells.
A diamantane derivative 1,6-Bis [4-(4-amino-3-hydroxyphenoxy) phenyl] diamantane (DPD) was found to inhibit the growth of several cancer cell lines in the National Cancer Institute (NCI) Anticancer Drug Screen system. In this study, we examined the in vitro and in vivo effects of DPD on human colon cancer cells. DPD exerted growth inhibitory activities in vitro against three human colon cancer cell lines (Colo 205,. DPD-treated cells were arrested at G 0 /G 1 as analysed by flow cytometric analysis. The expression of cyclin D was decreased in DPD-treated cells. The differentiation markers of carcinoembryonic antigen and fibronectin were significantly increased in colon cancer cells after treatment with DPD. The epithelium-like brush borders on HT-29 cell surface were also demonstrated at 1 week after withdrawal from DPD treatment. The DPD-induced cell growth inhibition and differentiation were irreversible after removal of DPD. The in vivo effect of tumour growth suppression by DPD was also observed in mouse xenografts. No acute toxicity was observed after an intraperitoneal challenge of DPD in BALB/c-nude mice weekly. These results suggest that DPD appears to be a new potentially less toxic modality of cancer therapy.
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